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    peter bondad

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    Post  peter bondad on Wed 12 Aug 2009, 11:33 pm

    CLASS,

    1. WHEN IS BIPOSY INDICATED IN CLIENTS SUSPECTED OF GN?
    2. WHAT IS THE BASIS OF DIETARY REGIMEN AMONG GN CLIENTS? WHAT ARE THE RESTRICTIONS?

    PLEASE PROVIDE STUDIES THAT SUPPORT YOUR RESPONSES.

    PROF. BONDAD
    gil_legarda
    gil_legarda

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    Post  gil_legarda on Sat 15 Aug 2009, 1:08 am

    BY: GIL LEGARDA
    ANSWER NO 1: According to this very recent study biopsy is indicated and used in the detection of pathogens in the kidney causing a polymavirus-associated nephrophaty for patients undergone kidney transplants.


    TITLE: Detection, Distribution, and Pathologic Significance of BK Virus Strains Isolated From Patients With Kidney Transplants, With and Without Polyomavirus-Associated Nephropathy
    BY: Boldorini, Renzo, Allegrini, Sara, Miglio, Umberto, Paganotti, Alessia, Veggiani, Claudia

    An experimental study to investigate the pathologic significance of BK virus strains and regulatory region sequence variations, to verify whether there are any differences in the frequency of BKV strains or TCR sequence variations between patients with kidney transplant, with and without PVAN; and to investigate whether the sequence analysis of the TCR of BKV can be used in the diagnosis or management of PVAN. Polyomavirus-associated nephropathy or PVAN is a tubular interstitial inflammatory disease caused by lytic infection of epithelial tubular cells by human BK polyomavirus or BKV in patients who have undergone kidney transplantation. There were 226 patients or subjects included in the study. From the patients developed PVAN, renal biopsy samples, 70 urine samples, and were taken, 63 blood samples and 682 urine samples, 677 blood samples, and 101 renal biopsy samples were taken from the control cases. Sequence analyses and amplification of regulatory region were obtained, and the sequences were analyzed using the Basic Local Alignment Search Tool program. Paired urine and blood samples were collected after renal transplantation to screen for, and monitor. The data collected were statistically analyzed using Fisher exact test, with P values <.05 considered significant 95% confidence interval.

    This research shows that WWT strain was frequently detected in PVAN cases than in control cases, and the AS and WW strains were only isolated from controls. The 128-1 strain was frequently associated with JC virus co-infection in both groups . Rearrangements of major WWT were detected in 29.6 percent of the urine samples, 30.4 percent of the blood samples, and one renal biopsy from the PVAN cases, but in only one urine sample from the controls. Although this study only shows 8 PVAN cases, the regulatory region sequence variations seem to be frequent and independent of the development of the disease, and the WWT strain seem to be more frequently related to the development of nephropathy than other strains.

    Most of the patients with BKV-JCV co-infection in both groups had rearranged BKV 128-1 strains. The significance of this finding is unknown, but it can be hypothesized that 128-1 which has never previously been reported in patients with renal transplants needs JCV co-infection to persist in patients with renal transplants or that there may be reciprocal interactions between the 2 PVs, similar to that reported for other viruses. The data indicate that BKV TCR sequence variations are frequent in patients with renal transplants regardless of the development of PVAN moreover, although the small number of patients with PVAN in the study does not allow any definite conclusions, the prevalence of the WWT strain in the renal tissue of patients with PVAN could suggest an association between it and the development of renal disease. Sequence analysis of the TCRs of BKV isolated from patients with renal transplants may be useful in predicting the possible development of renal damage but does not seem to be essential for a definite diagnosis of PVAN.

    Reference:
    Boldirini et al. (2009). Detection, Distribution, and Pathologic Significance of BK Virus Strains Isolated From Patients With Kidney Transplants, With and Without Polyomavirus-Associated Nephropathy. Archives of Pathology & Laboratory Medicine. Vol. 133, No. 5, pp. 766–774.
    http://arpa.allenpress.com/arpaonline/?request=get-document&doi=10.1043%2F1543-2165-133.5.766








    ANSWER NO 2: This research shows that L-arginine supplementation reduces fibrotic disease in ATS-induced glomerulonephritis if started after disease induction in combination with a low protein diet. A low protein diet would be recommended to our patients to prevent the occurrence of glumerulonephrities also hypertension will be prevented.

    TITLE: Tandem antifibrotic actions of L-arginine supplementation and low protein diet during the repair phase of experimental glomerulonephritis
    BY: Harm Peters, Wayne A Border and Nancy A Noble


    This an experimental study to identify the actions of L-argine supplementation and low protein diet during the repair phase from glumerulonephritis. Based upon the central role transforming growth factor-beta or TGF- over expression appears to play in renal fibrotic diseases, we have recently advocated reduction of TGF- as a therapeutic target. As part of efforts to determine the strength of this approach, we have undertaken studies to quantitate the effects of currently used and promising therapies in terms of their potential to reduce markers of disease in anti-thymocyte-serum or ATS-glomerulonephritis. The researchers assess the therapeutic effect of L-arginine supplementation, which has been shown to reduce fibrosis in a number of hypertensive models, given alone or in combination with low protein diet and started 24 hours after disease induction. Glomerulonephritis was induced by intravenous injection of OX-7 monoclonal antibody into 200 g Sprague-Dawley. Twenty-four hours later subjects were placed in groups that were either untreated, treated with 1% L-arginine in drinking water or 6% protein diets or both. On the day five of disease 24 hour urine specimens were collected and systemic blood pressure was measured. On the sixth day the subjects were anesthetized. Kidneys were perfused, tissue was taken for PAS staining and glomeruli were isolated. Aliquots of glomeruli were used for RNA preparation and for culture to determine 72-hour production of TGF- , fibronectin and plasminogen activator-type 1 or PAI-1, which was assayed by ELISA on culture supernatants.

    All disease measures except proteinuria and including matrix accumulation, TGF- , fibronectin and PAI-1 production and mRNA expression for TGF- , fibronectin and PAI-1 were significantly and similarly reduced by about 50% in groups treated with L-arginine or with low protein diet. Proteinuria was reduced in low protein treated but not in L-arginine supplemented subjects. Neither systemic blood pressure nor measures of NO synthesis showed differences between groups that could be attributed to L-arginine supplementation. Also disease-related increases in glomerular production of NOx were markedly reduced by low protein. The therapies which combined resulted in small but statistically significant decreases in most measures of disease.

    L-arginine supplementation reduces fibrotic disease in ATS-induced glomerulonephritis if started after disease induction. The absence of evidence for increased NO production related to L-arginine supplementation suggests that L-arginine is acting here through different pathways from those demonstrated in hypertensive models of disease. The data support the ideas that TGF- reduction is a valid therapeutic target and that quantitation of TGF- reduction is a useful approach for comparing antifibrotic drug candidates.


    Reference:
    Peters B. Et al. (2000). Tandem antifibrotic actions of L-arginine supplementation and low protein diet during the repair phase of experimental glomerulonephritis. Journal of the International Society of Nephrology. Vol. 57, pages 992–1001
    http://www.nature.com/ki/journal/v57/n3/abs/4491421a.html


    Last edited by gil_legarda on Mon 17 Aug 2009, 6:50 pm; edited 2 times in total
    alkhaloidz
    alkhaloidz

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    Post  alkhaloidz on Sun 16 Aug 2009, 9:02 pm

    # 1 ANSWER: Biopsy is indicated for suspected cases of GN when patients have an individual or family history of renal disease and when patients have an atypical presentation, including massive proteinuria, nephrotic syndrome, or a rapid rise in creatinine level without resolution. Biopsy is also indicated to patients who have a suspected recurrence of GN, basing from the study below:

    Glomerulonephritis Recurrence in the Renal Graft

    Renal transplantation is a treatment, not a cure. Although transplantation may return renal function to the recipient, it does not necessarily remove the cause of the recipient's original renal disease. Glomerulonephritis is the cause of renal failure for 20 to 40% of those who receive a transplant; for these recipients, the threat of recurrent disease is real. The transplant setting of immunosuppression, different antigenic characteristics of the graft versus the native kidney, and different chronology may attenuate or prevent recurrence of some forms of glomerulonephritis. Others will, despite these barriers, recur and may result in allograft failure.

    Allograft survival rates have steadily improved over the past 20 yr, largely as a result of our increasing ability to prevent and treat rejection (1). Recurrent glomerulonephritis is at present a minor contributor to allograft failure, responsible for 3% of all grafts lost in Australia and New Zealand from 1979 to 1998 (E. Briganti and S. Chadban, unpublished data) and a similar number in the United Kingdom (2). However, the propensity for glomerulonephritis to recur seems to be time dependent (3). Thus, as graft survival increases, so, too, does the likelihood of disease recurrence. As the average cadaveric graft is now projected to function for more than 13 yr and the average live-donor graft for more than 21 yr (1), we can expect to see an increased incidence of recurrent glomerulonephritis and a greater number of grafts failing as a result of recurrence.

    By implication, the diagnosis of recurrent glomerulonephritis requires an accurate diagnosis of both the primary renal disease and subsequent disease in the transplant kidney. In most cases, these criteria will be fulfilled only by obtaining renal biopsy material from both organs for diagnostic assessment, which may need to include electron microscopy and immunohistology (4,5). Although biopsy of native and transplant kidneys is simple, safe, and widely practiced, it is not performed in all cases of suspected glomerulonephritis in native or transplanted kidneys (6). Electron microscopy and immunohistology also are not routinely performed on transplant biopsies. Thus, the true incidence and impact of recurrent glomerulonephritis is not accurately known and is probably underestimated.

    Clinical Features and Differential Diagnosis of Recurrent Glomerulonephritis
    The typical features of recurrent glomerulonephritis are those of nephritis involving the native kidney, including proteinuria, hematuria, and deterioration in renal function. Renal function may be normal or impaired at the time of recurrence, and the rate of progression is extremely variable. Most important, recurrent glomerulonephritis may be one of several concurrent conditions that affect an allograft, with chronic allograft nephropathy or calcineurin-inhibitor toxicity commonly coexisting with glomerulonephritis. The presence of some forms of recurrent glomerulonephritis may actually predispose the graft to rejection, e.g., focal and segmental glomerulosclerosis (FSGS), and vice versa (15).

    For most types of recurrent glomerulonephritis, clinical features of the recurrence are similar to those of the primary disease. Extrarenal features of the primary condition may recur with recurrence in the transplant, such as thrombocytopenia and hemolysis in hemolytic uremic syndrome (HUS) and extrarenal vasculitis in recurrent Wegener's granulomatosis. Serology may be helpful in some cases, such as in anti—glomerular basement membrane (GBM) detection in Goodpasture disease, but may be variable in others, such as in recurrent lupus nephritis. Knowledge of hepatitis B or C antigenemia is important when considering recurrent membranous or mesangioproliferative glomerulonephritis.

    Renal biopsy is essential. When the diagnosis of recurrence is suspected, full evaluation of the biopsy specimen by light microscopy, immunohistology, and electron microscopy is desirable and in many cases essential (4,5). Light microscopy and immunohistology are necessary to differentiate recurrent from de novo glomerulonephritis, rejection, and calcineurin-inhibitor toxicity. The presence of tubulitis plus or minus vascular/glomerular changes should suggest acute rejection (16). Chronic rejection may produce chronic interstitial inflammation and glomerular changes, including cellular proliferation and basement membrane reduplication, which may be difficult to differentiate from mesangiocapillary glomerulonephritis (MCGN) by light microscopy (4,16). The use of immunohistology (content of deposits) and electron microscopy (location and structure of basement membrane and deposits) may clarify the diagnosis (4,5).

    Reference: Chadban, S. Glomerulonephritis Recurrence in the Renal Graft. Am Soc Nephrol 12:394-402. 2001

    # 2 ANSWER: The dietary regimen and restrictions of GN patients are based on the signs and symptoms exhibited by GN patients. based on the study below, it indicate that GN patients should monitor their sodium intake to prevent further progression of the condition.

    Renal adaptation to dietary sodium restriction in moderate renal failure resulting from chronic glomerular disease

    The renal response to sodium restriction was evaluated, and the concurrent changes of the plasma levels of aldosterone (ALDO) and atrial natriuretic peptide (ANP), in healthy patients (NOR), in normotensive patients with non-nephrotic chronic glomerulonephritis and normal renal function (GN), and in patients with glomerulonephritis and moderate renal failure (GFR, 41 +/- 4 mL/min; CRF). The three groups were studied for 1 wk after changing from a normal-sodium diet (NSD, 235 mEq NaCl/day) to a low-sodium diet (LSD, 35 mEq NaCl/day). All patients reached a steady sodium balance within the 4th and 5th day of LSD with an analogous cumulative loss of sodium. After salt restriction, the fractional urinary sodium excretion diminished by the same extent in the three groups, whereas the fractional free-water generation, measured during water diuresis, did not vary in NOR and markedly decreased in GN and CRF. Plasma levels of ALDO were similar in all groups at NSD and similarly increased during LSD. In GN and CRF, as compared to NOR, ANP levels were higher at NSD and decreased by a minor extent during LSD. Notably, in GN and CRF, but not in NOR, the attainment of the new sodium balance after sodium restriction was preceded by a significant parallel reduction of blood pressure and GFR; the GFR decline was secondary to a major decrement of RPF so that filtration fraction (FF) increased. It was concluded that in NOR, distal tubular effects of ANP and ALDO account for the attainment of sodium balance during LSD. As a difference, both GN and CRF patients achieve the new sodium balance primarily through hemodynamic changes: the renal hypoperfusion secondary to a decrease in blood pressure that diminishes the filtered load of sodium, and the increase of FF that enhances the proximal tubular sodium reabsorption. This abnormal response seems related to both the minor suppression of ANP and the increased salt-sensitivity of blood pressure that are likely the result of the presence of volume expansion.

    Reference: Cianciaruso, B et al. Renal adaptation to dietary sodium restriction in moderate renal failure resulting from chronic glomerular disease. Journal of the American Society of Nephrology, Vol 7, 306-313
    byron webb romero
    byron webb romero

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    Post  byron webb romero on Mon 17 Aug 2009, 1:42 pm

    Indications for Renal Biopsy in Glomerunephritis

    Although the health history, physical examination, urine analysis, and blood investigations may suggest a likely cause of glomerunephritis, definitive diagnosis of GN requires a renal biopsy. Underlying GN is also considered to be a cause of end stage renal failure in about a quarter of patients prescribed to dialysis programmes. As the progression of GN may be insidious, some patients present in chronic renal failure (CRF) with small smooth kidneys and by this time renal biopsy is more hazardous and is less likely to be informative so the precise diagnosis is often more difficult to confirm. The risk must always be weighted against the benefits despite the attraction of making a tissue diagnosis and rule out other related conditions. While the incidence of severe complications is low, the findings, especially in patients with mild disease, may be non-specific and would be of little prognostic value. Many nephrologists therefore carry out a renal biopsy only in patients in whom specific treatment is likely to be indicated or when assessment of prognosis is important. Mild hematuria and low level proteinuria (less than 2 g/day) in the absence of renal impairment or hypertension are associated with a good long term prognosis. Such patients can be safely managed with regular monitoring whereas an increase in proteinuria, the development of hypertension, or deterioration of renal function would then be indications for renal biopsy.

    Basis of Dietary Regimen and Restrictions for Patients with GN

    Patients with Glomerulonephritis should be prescribed with low sodium, normal protein diet. Glomerular diseases like that of GN, particularly the proliferative types are often associated with hypertension. Vigorous control of BP is important at every stage of management, and there is a strong impression that effective control slows the rate of progression of renal failure regardless of the underlying cause. Low protein diets have been recommended, but it is now apparent that protein restriction is of little value in most patients.

    Reference:
    Mason, P.D. & Pusey, C. D.Fortnightly Review: Glomerulonephritis: diagnosis and treatment. British Medical Journal. 1994;309:1557-1563 (10 December). Retrieved August 17, 2009, from http://www.bmj.com/cgi/content/full/309/6968/155.

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    guomanman
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    Post  guomanman on Mon 17 Aug 2009, 3:17 pm

    Background. Graft loss due to rejection is uncommon after human histocompatibility leukocyte antigen-identical living related donor (LRD) transplantation, resulting in an excellent long-term graft survival. Data on the impact of recurrence of the original disease on graft survival after LRD transplantation are scarce. Methods.We have studied the influence of recurrent glomerulonephritis in adult recipients of a human histocompatibility leukocyte antigen-identical LRD graft transplanted in our center in the period from 1968 to 1996. To that end, the data of 33 patients with proven or suspected primary glomerulonephritis and 27 patients with nonglomerular diseases were analyzed. Results. The patient survival was similar in both groups at 5, 10, and 20 years. The functional graft survival, i.e., graft survival after censoring for death, was, however, significantly worse for patients with glomerulonephritis as underlying disease (P<0.01). At 5 years graft survival was 100% vs. 88%, at 10 years 100% vs. 70%, and at 20 years 100% vs. 63%, respectively. Thus none of the patients with nonglomerular diseases lost a graft, whereas eight grafts were lost in the group of patients with glomerulonephritis. The main cause of graft loss in this patient group was recurrent glomerulonephritis (n=5), whereas chronic vascular rejection caused graft loss in two patients and occlusion of a transplant artery was the cause in one. A clinically significant proteinuria was detected in six more patients in the glomerulonephritis group: a recurrent glomerulonephritis was diagnosed in four patients and in two patients there was no biopsy. The cumulative incidence of recurrence was as high as 45% at 12 years after transplantation. Conclusion. Recipients of a human histocompatibility leukocyte antigen-identical LRD kidney have a good prognosis with respect to graft survival. After censoring for death, recurrent glomerulonephritis is the main cause of graft failure in these patients and the impact of recurrent disease on graft survival will become even more prominent with longer follow-up.

    Connie King, the nurse admitting Mr. Chang, notes that his history
    is essentially negative for past kidney or urinary problems.
    He relates having had a “pretty bad” sore throat a couple of
    weeks before admission.However, it was during midterms, so he
    took a few antibiotics he had from a previous bout of strep
    throat, increased his fluids, and did not see a doctor. The sore
    throat resolved, and he felt well until noticing the change in his
    urine. He admits that his eyes seemed a little puffy, but he
    thought this was due to lack of sleep and fatigue. He has eaten
    little the past 2 days, but was not alarmed because his food intake
    is irregular most of the time.
    Physical assessment findings include: T 98.8° F (37.1° C) PO, P
    98, R 18, and BP 136/90.Weight 165 pounds (75 kg), up from his
    normal of 160 (72.5 kg). Moderate periorbital edema and edema
    of hands and fingers noted.
    Throat culture is negative,but the ASO titer is high.CBC essentially
    normal. BUN 42 mg/dL, serum creatinine 2.1 mg/dL.
    Urinalysis reveals the presence of protein, red blood cells,and RBC
    casts.A subsequent 24-hour urine protein analysis shows 1025 mg
    of protein (normal 30 to 150 mg/24 hours).
    The physician diagnoses acute poststreptococcal glomerulonephritis
    and places Mr. Chang on bed rest with bathroom
    privileges. He orders fluid restriction (1200 mL/day) and a restricted
    sodium and protein diet.
    DIAGNOSIS
    Ms. King develops the following nursing diagnoses for Mr.Chang.
    • Excess fluid volume related to plasma protein deficit and sodium
    and water retention
    • Risk for imbalanced nutrition: Less than body requirements related
    to anorexia
    • Anxiety related to prescribed activity restriction
    • Risk for ineffective therapeutic regimen management related to
    lack of information about glomerulonephritis and treatment
    EXPECTED OUTCOMES
    The expected outcomes are that Mr.Chang will:
    • Maintain blood pressure within normal limits.
    • Return to usual weight with no evidence of edema.
    • Consume adequate calories following prescribed dietary limitations.
    • Verbalize reduced anxiety regarding ability to continue studies.
    • Demonstrate an understanding of acute glomerulonephritis
    and prescribed treatment regimen.
    PLANNING AND IMPLEMENTATION
    Ms. King plans the following nursing interventions for Mr.Chang.
    • Vital signs every 4 hours; notify physician of significant changes.
    • Weigh daily;intake and output every 8 hours.
    Schedule fluids allowing 650 mL on day shift, 450 mL on
    evening shift, and 100 mL on night shift.
    • Arrange dietary consultation to plan a diet that includes preferred
    foods as allowed.
    • Provide small meals with high-carbohydrate between-meal
    snacks.
    • Encourage Mr.Chang to talk about his condition and its potential
    effects.
    • Assist with problem solving and exploring options for maintaining
    studies.
    • Enlist friends and family to listen and provide support.
    • Teach Mr. Chang and his family about acute glomerulonephritis
    and prescribed treatment.
    • Instruct in appropriate antibiotic use.
    EVALUATION
    Mr.Chang is released from the infirmary after 4 days.He decides to
    return to his parents’home for the 6 to 12 weeks of convalescence
    prescribed by his doctor.Mr. Chang’s renal function gradually returns
    to normal with no further azotemia and minimal proteinuriaafter 4 months.He verbalizes understanding
    of the relationship between the strep throat,
    his inappropriate use of antibiotics, and the
    glomerulonephritis. He says,“I may not always remember to take
    every pill on time in the future, but I sure won’t save them for the
    next time again!”
    Critical Thinking in the Nursing Process
    1. How did Mr. Chang’s use of “a few” previously prescribed antibiotics
    to treat his sore throat affect his risk for developing
    poststreptococcal glomerulonephritis?
    2. What additional risk factors did Mr. Chang have for developing
    glomerulonephritis?
    3. The initial manifestations of acute poststreptococcal
    glomerulonephritis and rapidly progressive glomerulonephritis
    are very similar. What diagnostic test would the
    physician use to make the differential diagnosis? Develop a
    plan of care for a client undergoing this examination.
    joanalyn_balino
    joanalyn_balino

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    Post  joanalyn_balino on Mon 17 Aug 2009, 11:17 pm

    Question 1

    WHEN IS BIOPSY INDICATED IN CLIENTS SUSPECTED OF GN?

    Renal biopsy is done to identify specific histopathologic pattern of glomerular injury. Indications: Microscopic haematuria with dysmorphic red cells or casts, a possible hereditary condition, associated proteinuria, hypertension or reduced glomerular filtration rate, with sudden unexplained reduction of glomerular filtration rate or unexplained increased proteinuria. It provides valuable information when evaluating the activity of the renal vasculitis and that it is important for the therapeutic management(Ferrario,Rastaldiand and Amico, 1996).


    Question 2

    WHAT IS THE BASIS OF DIETARY REGIMEN AMONG GN CLIENTS? WHAT ARE THE RESTRICTIONS?

    Dietary regimen among GN clients will be based on the current kidney function and their special dietary needs. There is only Minimal restrictions for mild impairment of kidney function, while advanced kidney disease may require severe restrictions on the amounts of protein, sodium, potassium, phosphorus and fluids.Fouque, Wang, Laville, Boissel made a A systematic review of published literature (clinical trials) from 1975to 1999 to determine the efficacy of low protein diets in preventing the natural progression of chronic renal failure towards end-stage renal disease and therefore delaying the need for starting maintenance dialysis. All of the patients (subjects) were suffering from moderate to severe chronic renal failure. The type of intervention given was Standard protein intake (0.8 g/kg/day) or greater versus a moderate (0.6 g/kg/day) to severe protein restriction (0.3 g/kg/day) regardless of supplementation with essential amino acids or ketoacids. They concluded that by reducing the protein intake in patients with chronic renal failure reduces the occurrence of renal death by about 40% as compared with larger or unrestricted protein intake.

    References
    Papanagnou, D., Kwon, N. (2008) Glomerulonephritis, Acute: Differential Diagnoses and workup. Emedicine. Retrieved August 16, 2009 from http://emedicine.medscape.com/article/777272-diagnosis


    Fouque,D., Wang,P., Laville,M., Boissel, J.P..(2000). Low protein diets delay end-stage renal disease in non-diabetic adults with chronic renal failure. Nephrol Dial Transplant 15: 1986-1992. RetrievedAugust 17, 2009 from http://ndt.oxfordjournals.org/cgi/reprint/15/12/1986?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=Low+Protein+diet+delay+end+stage+renal+disease&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT

    Ferrario F, Rastaldi MP, D'Amico G. The crucial role of renal biopsy in the management of ANCA-associated renal vasculitis. Nephrol Dial Transplant1996; 11: 726–728. Retrieved August 17, 2009 from http://ndt.oxfordjournals.org/cgi/reprint/11/4/726?ijkey=29a45b3a083bf4b27407b62eeedfb1b1b45f5172&keytype2=tf_ipsecsha


    Last edited by joanalyn_balino on Tue 18 Aug 2009, 3:18 am; edited 1 time in total
    monchRN
    monchRN

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    Post  monchRN on Tue 18 Aug 2009, 12:36 am

    ANSWER:

    Biopsy indicated for client with familial history of renal disease and those clients with atypical presentation with presenting signs and symptoms of renal insufficiency.


    Patients who are candidates for renal biopsy are those with individual, or familial history of renal disease, as well as patients with atypical presentation (includes proteinuria, nephritic syndrome, or a rapid rise in the level of creatinine without resolution). Fuiano, et.al (2001), mentioned that when patients are presenting with signs and symptoms of renal insufficiency, renal biopsy establishes a pathologic diagnosis.

    Certain considerations are however taken into account such as the kidney size or the extent of kidney insufficiency prior to undergoing a renal biopsy. As for patients with severe chronic insufficiency, undergoing this procedure poses additional complications and seems futile as this would not affect management of the condition. But for mild to moderate renal insufficiency, the procedure may identify the causes of the problem and may alter the treatment course. For acute renal insufficiency, biopsy still remains important. IgA nephropathy (IgAN) was the most common glomerulonephritis at renal biopsy in a study conducted by Coppo, Gianoglio, Porcellini, and Maringhini (1998).

    References:

    Coppo, R., Gianoglio et. al. (1998). Frequency of renal diseases and clinical indications for renal biopsy in children (Report of the Italian National Registry of Renal Biopsies in Children. Nephrology Dialysis Transplantation. 13: 294-297. Retrieved on August 17, 2009, from http://ndt.oxfordjourbals.org/cgi/reprint/13/2/291

    Fuiano, G.,et. al. (2001). Renal Biopsy: Clinical Indications. Italy: Chai of Nephrology. Retrieved on August 17, 2009, from: http://www.unimet.edu/cin2001-old/conf/fuiano.html
    rodel_perez_rn
    rodel_perez_rn

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    Post  rodel_perez_rn on Tue 18 Aug 2009, 10:38 pm

    Answer to Question 1:

    The present study conducted by SN Wong, KW Chan, MC Chiu, HK Paediatric Nephrology Study Group (2007) surveyed children with renal diseases in Hong Kong on the role of renal biopsy in the diagnostic evaluation of the disease. Renal biopsy were not performed by nephrologists for children with nephrotic syndrome, atypical features such as gross hematuria, hypertension, impaired renal function and low complement levels.

    The expected result from the selective approach done to biopsy, children biopsied for GN had a small percentage of minimal disease changes compared to unselected cases. Most patients biopsied for an age of onset of > 10 years or for steroid dependence or late steroid resistance have either MCD or DMP or FSGS. Results support the argument that a renal biopsy is not mandatory in the nephrotic children above 10 years of age, before steroid treatment, or those children with steroid sensitive but dependent nephrotic syndrome before receiving cyclophosphamide.

    Renal biopsy was also done to children with microscopic hematuria after a period of observation and if parents were anxious to know the cause. Most likely the causes in the patients with recurrent gross hematuria were IgA nephropathy, benign recurrent hematuria or Alport's syndrome. There is at present no specific therapy for mild IgA nephropathy or benign recurrent hematuria. For Alport's syndrome, no therapy can alter the progressive course. Therefore renal biopsy in this situation only provides information for the prediction of prognosis for the anxious parents.

    On the other hand, patients with proteinuria and hematuria with or without other nephritic features were biopsied, a variety of glomerulonephritis were found. Some of these, such as anti-GBM crescentic nephritis, membranoproliferative glomerulonephritis, need early specific treatment. A renal biopsy is definitely indicated early in the course of this group of patients.

    In conclusion, pediatric nephrologists in Hong Kong adopt a selective approach in performing renal biopsies. While minimal change disease is the commonest pathology, population has a higher prevalence of DMP and HBV-associated membranous nephropathy among the nephrotic children in Hong Kong. The commoner causes of persistent hematuria are IgA nephropathy, Alport's syndrome and benign hematuria. Lupus nephritis and Henoch-Schonlein nephritis are the two commonest systemic diseases causing secondary glomerulonephritis.

    References:

    Iversen P. Brun C. Aspiration biopsy of the kidney. Am J Med 1951;11:324-30.

    Habib R. A story of glomerulopathies: a pathologist's experience. Pediatr Nephrol 1993;7:336-46.

    Lai KN, Lai FM, Chan KW, Au TC, Tam A, Leung NK. Pattern of glomerulonephritis in Chinese population: The effect of renal biopsy on the therapeutic decision. Aust Paediatr J 1987;23:231-4.
    Chan KW, Chan PCK, Cheng KP, Man MK. Pathology of glomerular diseases in Hong Kong. J Hong Kong Med Assoc 1989;41:355-8.

    Churg J, Bernstein J, Glassock RJ. Renal disease: classification and atlas of glomerular diseases. 2nd Ed., Igaku-Shoin, New York, 1995.

    Information Support Unit, Hospital Authority. Hospital Authority Statistical Report 1992/93, Government Printer, Hong Kong, pp 67, 1993.

    International Study of Kidney Disease in Childhood. The nephrotic syndrome in children: prediction of histology from clinical and laboratory characteristics at the time of diagnosis. Kidney Int 1978;13:159-65.

    Answer to Question 2:

    It has been proven that food-source of circulating immune complexes (CICs) contribute to some kidney problems. Glomerulonephritis, a serious kidney inflammation, is one disease which may sometimes be triggered by CICs which has food protein antigens. It has been suggested that recurring triad of signs and symptoms which are flank pain, blood or protein in urine are caused by “food allergy” until proven otherwise. Hence, diet which exclude antigenic material should be implemented (i.e. Alpha ENF which is a diet program offered to supplement those nutrients such as amino acids, Vit B, D, B12 and minerals such as calcium, magnesium, potassium, and zinc). . It is advisable that patients with kidney disease should eat low protein foods to decrease demands on deteriorating kidney function.

    Likewise, nephrotic syndrome, which involves increased glomerular excretion of protein should also be advised to modify diet containing low-protein foods. In a case study (Gabordi, et al), a 6 yr old girl with nephritic syndrome, celiac disease and dermatitis herpetiforms was cured when gluten grains was removed from her diet. In another case by Sandberg et al, 6 patients had remission from nephrotic syndrome when milk was removed from their diet and had exacerbation when it was reintroduced. Also, 6 out of 17 children with steroid resistant nephrotic syndrome had remission of proteinuria in 3-8 days when milk removed from their diet. Using dietetic therapy to prevent further deterioration of kidney function is further reinforced by a study done by Ferri, et al (1993) on dietary macromolecular antigens which can be associated in the pathogenesis of IgA nephropathy (IgAN). The study was about the effect of a low-antigen-content diet of 21 patients with active IgAN. It was discovered that heavy proteinuria in 12 cases was decreased or has disappeared in 11 patients after the diet therapy.

    These studies just prove that what appears to be very difficult to cure complex kidney diseases may be controlled or health of the patient may be improved by just adhering to a simple diet program specifically tailored to a particular kidney disease (ex. glomerulonephritis and nephritic syndrome). These studies reinforce the fact that following a low protein diet and avoiding food-source of circulating immune complexes (CICs) may greatly control and enhance the function of the kidneys. For patients with kidney problems, it is vital that they are referred to kidney dietician in order to have a diet program that is tailored to their current health condition in order to reduce workload of their damaged kidneys.

    References:
    Ferri C; Puccini R; Longombardo G; Paleologo G; Migliorini P; Moriconi L; Pasero G; Cioni L. Low-antigen-content diet in the treatment of patients with IgA nephropathy. Nephrol Dial Transplant, 1993, 8:11, 1193-8.
    Jackson S; Moldoveanu Z; Kirk KA; Julian BA; Patterson TF; Mullins AL; Jilling T; Mestecky J; Galla JH. IgA-containing immune complexes after challenge with food antigens in patients with IgA nephropathy. Clin Exp Immunol, 1992 Aug, 89:2, 315-20
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    VonDeneb_Vitto

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    Post  VonDeneb_Vitto on Wed 19 Aug 2009, 12:37 pm

    WHEN IS BIPOSY INDICATED IN CLIENTS SUSPECTED OF GN?

    In a report of the Italian National Registry of Renal Biopsies in Children, Italian children underwent renal biopsy because of isolated microscopic haematuria with 19.3%, non-nephrotic proteinuria with or without microscopic haematuria with 31.2%, and nephrotic-range proteinuria with 34.2%.

    Reference:
    Coppo, R., Gianoglio, B., Porcellini, M., & Maringhini, S. (1998). Frequency of renal diseases and clinical indication for renal biopsy in children (Report of the Italian National Registry of Renal Biopsies in Children). Nephrology Dialysis Transplantation (1998). 13 (2) 291-295. Retrieved August 18, 2009, from http://ndt.oxfordjournals.org/cgi/reprint/13/2/291.


    WHAT IS THE BASIS OF DIETARY REGIMEN AMONG GN CLIENTS? WHAT ARE THE RESTRICTIONS?

    Clinically, hematuria and low-grade proteinuria are the first sign of recurrence of IgA glomerulonephritis. European Renal Association-European Dialysis and Transplant Association advised ACE inhibitors, fish oil, and tight blood pressure control to be equitable dealings to slow down the development of recurrent disease.

    Cheng and colleagues investigated the effect of fish-oil dietary supplement on the rate of progression of renal failure in 11 patients with IgA nephropathy by comparing the slope of the plot of reciprocal serum creatinine versus time before and after supplement. The result of the study showed that non-immune factors probably contribute to progression of renal failure in patients with IgA nephropathy, and fish oil dietary supplement has either no demonstrable or an unpredictable effect.

    References:

    Late recurrence of primary glomerulonephritides. Nephrology Dialysis Transplantation (2002) 17: 16-18. Retrieved August 18, 2009, from http://ndt.oxfordjournals.org/cgi/reprint/17/suppl_4/16?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=glomerulonephritis+diet+therapy&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT

    Cheng, I. K. P., Chan, P. C. K., Chan, M. K. (1990). The Effect of Fish-Oil Dietary Supplement on the Progression of Mesangial IgA Glomerulonephritis. Nephrology Dialysis Transplantation (1990) 5: 241-246. Retrieved August 18, 2009 from http://ndt.oxfordjournals.org/cgi/reprint/5/4/241?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=fish+oil+treatment+gor+glomerulonephritis&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT
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    Post  *alexus on Thu 20 Aug 2009, 5:00 pm

    1. WHEN IS BIPOSY INDICATED IN CLIENTS SUSPECTED OF GN?

    A kidney biopsy can help in forming a diagnosis and in choosing the best course of treatment. A kidney biopsy may be recommended for any of the following conditions:
    • hematuria, which is blood in the urine
    • proteinuria, which is excessive protein in the urine
    • impaired kidney function, which causes excessive waste products in the blood

    A pathologist will look at the kidney tissue samples to check for unusual deposits, scarring, or infecting organisms that would explain a person’s condition. The doctor may find a condition that can be treated and cured. If a person has progressive kidney failure, the biopsy may show how quickly the disease is advancing. A biopsy can also help explain why a transplanted kidney is not working properly.

    Referrence:
    National Kidney and Urologic Diseases Information Clearing house (NKUDIC)

    2. WHAT IS THE BASIS OF DIETARY REGIMEN AMONG GN CLIENTS? WHAT ARE THE RESTRICTIONS?

    During glomerulonephritis, the glomeruli become inflamed and impair the kidney's ability to filter urine.
    If glomerulonephritis is caused by a streptococcal infection, then treatment will be focused on curing the infection and treating the symptoms associated with the infection. Unfortunately, glomerulonephritis caused by a different reason cannot be cured. Therefore, treatments focus on slowing the progression of the disease preventing complications.
    Treatment for glomerulonephritis may include:
    • fluid restriction
    • decreased protein diet
    • decreased salt and potassium diet
    • medication, such as:
    o diuretics
    o blood pressure medications
    o phosphate binders - medications to decrease the amount of the mineral phosphorus in the blood.
    o immunosuppressive agents.

    Referrence:
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    YangChunHua

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    Post  YangChunHua on Fri 21 Aug 2009, 2:43 am

    Answer:2. WHAT IS THE BASIS OF DIETARY REGIMEN AMONG GN CLIENTS? WHAT ARE THE RESTRICTIONS?
    A person with acute glomerulonephritis may need to avoid some foods and limit the amount of others. Waste products that failing kidneys cannot handle include protein, sodium, potassium, and phosphorus.

    General Dietary Restrictions
    When the kidneys are not working normally, waste products (blood urea nitrogen), the result of what we eat, build up in the bloodstream. Kidney dialysis (kidney machine) removes part of these byproducts temporarily until, once again, they accumulate. It is important for both the patient who is dependent upon dialysis, or suffering from compromised kidney function, to follow a carefully outlined diet. Typical dietary restrictions will be placed on total calories, fluids, protein, sodium, phosphorus, and potassium. Supplemental calcium is also required by many patients.
    http://www.freemd.com/acute-glomerulonephritis/home-care-kidney-diet.htm
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    Post  yachen on Fri 21 Aug 2009, 4:23 am

    answer:

    2/Chronic glomerulonephritis, also known as chronic nephritis, is a combination of reasons, a variety of pathological types of the primary glomerular a group of autoimmune diseases. The general course of a long to clinical proteinuria, hematuria, edema, hypertension and renal insufficiency characterized. Treatment of the disease is a comprehensive course of treatment, although drug therapy is important, but also in patients with essential dietary conditioning.
    Control of salt: mild edema, high blood pressure are advised to enter low-salt diet, salt is no more than 3 grams / day. If a high degree of edema, they should be into the non-salt diet. No edema and hypertension are optional ordinary diet, and it is not too Chatham. Protein intake: the intake of protein to supplement your body needs. In the absence of edema, hypertension and normal renal function, the daily protein supplement daily urine protein loss × 1.45 +1.0 g / kg body weight, including high quality protein (ie animal protein) accounted for 50% and, if renal insufficiency , a daily supplement of protein 0.6 to 0.8 g / kg body weight, which accounted for 75% of high quality protein.
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    Post  nancelle on Fri 21 Aug 2009, 11:20 am

    Nancelle Grace G. Dumlao

    Glomerulonephritis Thread:


    1. WHEN IS BIPOSY INDICATED IN CLIENTS SUSPECTED OF GN?
    2. WHAT IS THE BASIS OF DIETARY REGIMEN AMONG GN CLIENTS? WHAT ARE THE RESTRICTIONS?

    PLEASE PROVIDE STUDIES THAT SUPPORT YOUR RESPONSES.

    ANSWER 1: 1. WHEN IS BIPOSY INDICATED IN CLIENTS SUSPECTED OF GN?

    Glomerulonephritis (GN) is a kidney disease that presents in many different ways and accurate diagnosis can be difficult. Certain signs and symptoms may suggest GN but normally it is discovered when a urine urinalysis is not normal (with RBC or casts could mean glomerular damage; WBC means infection, increased protein du e to nephron damage). GN may be also be diagnosed using history, examination, blood tests (creatinine and urea) and even hard-to-control high blood pressure, but a definitive diagnosis can be achieved using renal biopsy.

    GN is one of the major causes of CRF and since the progression of GN is such that the disease is already established before it becomes apparent, the kidneys of CRF patients may become small smooth kidneys (nephrosclerosis). At this point, renal biopsy in no longer advisable since it could be more dangerous to the patient. Hence, many nephrologist order renal biopsy only for patients who will benefit in specific treatments and when knowing the prognosis is vital. For instance, those patients with good prognosis such as those with mild hematura and low level proteinuria (less than 2g/day) with no renal impairment nor hypertension, they may be managed with regular check-ups. However, if the patient has increased proteinuria, hypertension or there is deterioration in kidney function, then renal biopsy is strongly indicated (Mason, 1994).

    In a review of several studies done by Cohen and Brown (2003), they explored the significance of microscopic hematuria as initial warning sign for underlying diseases such as glomrulonephritis, other kidney disease, cystitis and other illnesses. They also reviewed previous studies on when microscopic hematuria should be followed by other diagnostic tests or when it may be safe to say that it is from benign causes (eg. Exercise, menstruation).

    The study is quite long but let me just focus on its finding regarding the use of renal biopsy to further confirm the existence of glomerular damage.

    Microscopic hematuria without proteinuria can either be of glomerular or nonglomerular (could involve the kidney and upper urinary tract) origin. If with microscopic hematuria, renal biopsy is not a routine follow-up test and thus, it cannot be determined if bleeding is from the glomeruli. In one study involving 157 men with microscopic hematuria whose cause could not be identified, the use of renal biopsy helped identified that bleeding in 16% of these men was due to a glomerular source. In another study with 165 patients, renal biopsy w as performed for each patient after renal imaging and cystoscopy. Renal biopsy was helpful in confirming that 87 patients had no abnormalities and 49 had IgA nephropathy.

    Microscopic hematuria as mentioned above is the initial warning for glomerular bleeding. Further tests should be done to ascertain that renal insufficiency is present and they may be referred to a nephrologist for evaluation and possible renal biopsy. Referral should be immediate especially if second test of serum creatinine is abnormal or higher than the first result. However the indication for renal biopsy if microscopic hematuria is not accompanied by significant proteinuria or renal insufficiency is not supported due to the limited data available. But it was stressed that renal biopsy is indicate if the result could make a difference in the management or care of the illness.

    Reference:

    Cohen,R.A., and Brown R.S. Microscopic Hematuria. The New England Journal of Medicine. June, 2003; volume 348:2330-2338.

    Mason, P.D., Pusey, C.D. Fortnightly Review: Glomerulonephritis: diagnosis and treatment. BMJ. December, 1994, 309:1557-1563.


    ANSWER 2:
    WHAT IS THE BASIS OF DIETARY REGIMEN AMONG GN CLIENTS? WHAT ARE THE RESTRICTIONS?


    Several studies purport the low protein diet regimen for patients with kidney damage (GN and CKD among others). In the study below by Ideura, Shimazui, Morit, and Yoshimura in 2007, the authors further indicated that protein intake of more than 0.5 g/kg BW/day is no longer effective in controlling the further deterioration of chronic kidney failure.

    However, it is still strongly recommended that patients with kidney problems should be referred to a kidney dietician for a diet regimen that is tailored to their current health condition so as to reduce the workload of their damaged kidneys.


    In glomerulonephritis, there is serious kidney inflammation which may sometimes be triggered by circulating immune complexes (CIC) that may increase when large protein food molecules are released into the blood through the digestive tract. Hence, the limitation in protein intake is highly recommended.

    The kidneys are susceptible to structural damages due to the various blood components being filtered on a daily basis. One cause of damage is the circulating immune complexes (CIC) which may increase when large protein food molecules are released into the blood through the digestive tract. Since the cause of the problem is the food that we take in, then this problem may also be resolved by controlling the kind of food that we eat. Through the years, there are numerous studies conducted to understand what foods may have damaging effects on the kidneys (Ferri, et al, 1993; Jackson, et al, 1992; Coppo, et al, 1991; Rostoker, et al, 1991). It has been proven that food-source of circulating immune complexes (CICs) contribute to some kidney problems. Glomerulonephritis, a serious kidney inflammation, is one disease which may sometimes be triggered by CICs which has food protein antigens. It has been suggested that recurring triad of signs and symptoms which are flank pain, blood or protein in urine are caused by “food allergy” until proven otherwise. Hence, diet which exclude antigenic material should be implemented (i.e. Alpha ENF which is a diet program offered to supplement those nutrients such as amino acids, Vit B, D, B12 and minerals such as calcium, magnesium, potassium, and zinc). . It is advisable that patients with kidney disease should eat low protein foods to decrease demands on deteriorating kidney function.
    It is believed that proteins in general are high-risk food components in kidney disease and hydrolyzed proteins may have harmful effects. High protein foods that are excluded in the Alpha ENF list include gluten, the proteins in wheat, rye, barley and oats. Other high-protein foods are albumin from eggs and milk, muscle proteins from meat, globulin and casein from milk, and soy proteins. However, proteins from vegetables are better tolerated and maybe included in kidney diet.
    A low protein diet and avoiding food-source of circulating immune complexes (CICs) may greatly control and enhance the function of the kidneys.

    Protein Intake of More than 0.5 g/kg BW/Day Is not Effective in Suppressing the Progression of Chronic Renal Failure

    By: Ideura T, Shimazui M, Morita H, Yoshimura A (2007)

    This is a study was undertaken to identify how much protein should a patient with chronic renal failure (CRF) include in their diet. As mentioned above, it is well-known that protein restriction in the diet of CRF patients helps in controlling the progressive loss of kidney function, but there are no solid basis to support if this is really beneficial. In fact, there is still an issue regarding the amount of protein intake that could lead to positive outcome. Hence, this study was undertaken to identify the correct protein restriction that could translate to positive outcomes for patients with kidney disease. The sample included 121 patients with chronic glomerulonephritis (CGN) with serum creatinine level of 6mg/dl and they were further divided into six groups with corresponding amounts of protein restriction in their diet (e.g, 0.3 g/kg BW/day (0.3 g), 0.4, 0.5, 0.6, 0.7, and 0.8 g). The rate of decline in creatinine clearance were based on the whether kidney function deteriorates. Also, 24-hour urine sample was used to estimate the amount of protein intake as reflected by the appearance of urea nitrogen in the urine.

    The study yielded significant information regarding the amount of protein intake that would have a beneficial effect on the kidney patient. It revealed that progression of renal dysfunction is suppressed for control groups with protein restriction in their diet of 0.5-, 0.4-, and 0.3-g groups. For those taking more than 0.6g of protein in their diet, there was no significant changes in the kidney dysfunction. They conclude that protein intake of more than 0.5g/kg BW/day is not effective in slowing down the deterioration of kidney function in CRF arising from chronic glomerulonephritis.


    References:
    Ideura T, Shimazui M, Morita H, Yoshimura A. Protein Intake of More than 0.5 g/kg BW/Day Is not Effective in Suppressing the Progression of Chronic Renal Failure. Nutrition and Kidney Disease: A New Era. Contrib Nephrol. Basel, Karger, 2007, vol 155, pp 40-49 (DOI: 10.1159/000100995)

    Ferri C; Puccini R; Longombardo G; Paleologo G; Migliorini P; Moriconi L; Pasero G; Cioni L. Low-antigen-content diet in the treatment of patients with IgA nephropathy. Nephrol Dial Transplant, 1993, 8:11, 1193-8.
    Jackson S; Moldoveanu Z; Kirk KA; Julian BA; Patterson TF; Mullins AL; Jilling T; Mestecky J; Galla JH. IgA-containing immune complexes after challenge with food antigens in patients with IgA nephropathy. Clin Exp Immunol, 1992 Aug, 89:2, 315-20
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    Post  Lucy Yuan on Fri 21 Aug 2009, 9:19 pm

    answer question 1
    A kidney biopsy is the most reliable way to distinguish chronic glomerulonephritis from other kidney diseases. A biopsy, however, is rarely done in advanced stages. In these cases, the kidneys are shrunken and scarred, and the chance of obtaining specific information about the cause is small. Doctors suspect that the kidneys are shrunken and scarred if kidney function has been poor for a long time and the kidneys appear abnormally small on an imaging test.

    relevent article:GlomerulonephritisRecurrenceintheRenalGraft
    STEVENJAMESCHADBAN
    DepartmentofNephrology,MonashMedicalCentre,Clayton,Australia.


    answer question2
    NONPHARMACOLOGIC THERAPY

    • Avoidance of salt if edema or hypertension is present
    • Low-protein intake (approximately 0.5 g/kg/day) in patients with renal failure
    • Fluid restriction in patients with significant edema
    • Avoidance of high-potassium foods
    Amelioration of experimental glomerulonephritis by dietary protein restriction.Neugarten J, Feiner HD, Schacht RG, Baldwin DS.
    We have examined the effects of various levels of dietary protein intake on the course of nephrotoxic serum nephritis in the rat by feeding low (4.6% casein), standard (23% casein), and high (57.5% casein) protein diets which were identical in calorie, mineral, and electrolyte content. Nephritic rats on a high protein diet manifested heavy proteinuria, hypoalbuminemia, hypercholesterolemia, azotemia, and elevated serum creatinine levels. In those subjected to dietary protein restriction, proteinuria remitted and azotemia did not develop. While mesangial widening, interstitial abnormalities, and segmental proliferation and sclerosis of glomeruli occurred regularly in nephritic rats fed high protein diets, histologic abnormalities were virtually absent in those on low protein intake. Animals on a standard protein intake manifested histologic and clinical features intermediate in severity. We conclude that the renal functional and histologic consequences of nephrotoxic serum nephritis can be averted by dietary protein restriction.


    relevent article:

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