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Year : 2016  |  Volume : 29  |  Issue : 4  |  Page : 765-771

Management of nephrotic syndrome in family practice: a systematic review

1 Department of Internal Medicine, Faculty of Medicine, Menoufia University, Menoufia, Egypt
2 Department of Family Medicine, Faculty of Medicine, Menoufia University, Menoufia, Egypt
3 Department of Family Medicine, Ministry of Health, Menoufia Governorate, Egypt

Date of Submission04-Jan-2015
Date of Acceptance06-Mar-2015
Date of Web Publication21-Mar-2017

Correspondence Address:
Basma A Hafez El Beah
Menouf, El-Menoufia, 32951
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1110-2098.202532

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The aim of the study was to perform a systematic review to summarize the diagnosis and management of nephrotic syndrome in family practice.
Data sources
Medline, articles in Medscape, American Family Physician (AAFP), and PubMed were searched. The search was performed on 1 November 2014 and included all articles with no language restrictions.
Study selection
The initial search yielded 250 articles. Six articles fulfilled the inclusion criteria. The articles included nephrotic syndrome clinical presentation, investigation to confirm the diagnosis, and management in family practice.
Data extraction
Data from each eligible study were abstracted independently in duplicate using a data collection form to obtain information on study characteristics, interventions, and quantitative results reported for each outcome of interest.
Data synthesis
There was heterogeneity in the data collected. A meta-analysis could not be carried out. Significant data were collected. Thus, a structured review was performed.
Six articles were reviewed; five articles and one systematic review summarize the clinical presentation investigation and management. Patients with nephrotic syndrome present with marked edema, proteinuria, hypoalbuminemia, and often hyperlipidemia. In adults, diabetes mellitus is the most common secondary cause, and focal segmental glomerulosclerosis and membranous nephropathy are the most common primary causes. Family physicians may encounter patients with nephrotic syndrome because of primary renal disease or a number of secondary causes, and should initiate appropriate diagnostic workup and medical management pending specialist consultation.

Keywords: hyperlipidemia, hypoalbuminemia, idiopathic, nephrotic syndrome, proteinuria

How to cite this article:
Kora MA, Shahin HM, Khalil NA, Hafez El Beah BA. Management of nephrotic syndrome in family practice: a systematic review. Menoufia Med J 2016;29:765-71

How to cite this URL:
Kora MA, Shahin HM, Khalil NA, Hafez El Beah BA. Management of nephrotic syndrome in family practice: a systematic review. Menoufia Med J [serial online] 2016 [cited 2022 Jul 5];29:765-71. Available from: http://www.mmj.eg.net/text.asp?2016/29/4/765/202532

  Introduction Top

Nephrotic syndrome is a disorder that indicates damaged kidneys. It refers to a group of symptoms, including protein in the urine, low blood protein, and high cholesterol. Nephrotic syndrome can develop in any individual. Nephrotic syndrome can be caused by infection, the side effects of medication, heredity, cancer, and autoimmune disorders, such as diabetes and lupus [1].

The nephrotic syndrome is defined by heavy proteinuria because of an abnormal increase in glomerular permeability and following hypoalbuminemia, hyperlipidemia, and edema. Most patients with nephrotic edema have primary salt retention. Overproduction and impaired catabolism of lipoproteins are the causes of hyperlipidemia. Abnormality of coagulation factors is also associated with nephrotic syndrome [2].

Nephrotic syndrome may be primary or secondary to systemic disorders. Once diagnosed, the cause for the nephrotic syndrome must be examined. Other symptoms and signs of nephrotic syndrome are foamy urine, unexplained weight gain, loss of appetite, high blood pressure, and edema, especially in the face, feet, and abdomen. Treatment for nephrotic syndrome is aimed at controlling these symptoms [1],[3].

It has serious complications and must be on the differential diagnosis for any patient presenting with new-onset edema. Assessment for the underlying cause of nephrotic syndrome is essential [4].

Nephrotic syndrome may be treated with blood pressure medications, such as angiotensin receptor blockers and angiotensin-converting enzyme inhibitors. Immunosuppressant drugs and drugs to treat high cholesterol may also be used depending on the cause. Proper medical treatment may help prevent further damage to the kidneys [5].

Family physicians may encounter patients with nephrotic syndrome because of primary (idiopathic) renal disease or a number of secondary causes, and should initiate appropriate diagnostic workup and medical management pending specialist consultation [6].

  Materials and Method Top

This review was performed according to the guidelines developed by the center for review and dissemination. It was used to assess the methodology and outcome of the studies.

Search strategy

A search was performed in several databases. It included Medline, articles in Medscape, American Family Physician (AAFP), and PubMed. The search was performed on 1 November 2014 and included all articles published. There was no restriction according to language.

Study selection

All researches were assessed for inclusion in the review by three researchers. They were included if they fulfilled the following criteria:

  • Definition of nephrotic syndrome
  • Clinical presentation of nephrotic syndrome
  • Diagnosis and investigation of nephrotic syndrome
  • Management of nephrotic syndrome.

Participants: adults with nephrotic syndrome were included in this study.

Intervention: early investigation and management.

Comparative: manifested nephrotic syndrome.

Outcome: proper health.

Articles that were not in English were translated. The article title and abstract were initially screened. Then, the selected articles were read in full and further assessed for eligibility. All references from the eligible articles were reviewed to identify additional studies.

Data extraction

Data from each eligible study were abstracted independently in duplicate using a data collection form to capture information on study characteristics, interventions, and quantitative results reported for each outcome of interest. Conclusion and comments were made on each study.

There was heterogeneity in the data collected. A meta-analysis could not be carried out. Significant data were collected. Thus, a structured review was performed, with tabulation of the results.

  Result Top

Six studies were selected. The studies were considered eligible if they fulfilled the inclusion criteria. There was a high degree of heterogeneity in the diagnosis and management of nephrotic syndrome.

  Discussion Top

According to Cameron and Hicks [7], the nephrotic syndrome was defined as one of the best-known presentations of adult or pediatric kidney disease. The term describes the association of proteinuria with peripheral edema, hypoalbuminemia, and hypercholesterolemia ([Table 1]). Protein in the urine (coagulable urine) was first described in 1821. According to Jayawardene et al. [8], it is a relatively rare manifestation of kidney disease compared with reduced kidney function or microalbuminuria as a complication of systemic diseases, such as diabetes and elevated blood pressure. According to Kitiyakara et al. [6], most cases of nephrotic syndrome appear to be caused by primary kidney disease. [Table 2] summarizes the recognized histologic patterns and features of primary nephrotic syndrome. Membranous nephropathy and focal segmental glomerulosclerosis (FSGS) each account for about one third of cases of primary nephrotic syndrome. According to Hull and Goldsmith [4], FSGS is the most common cause of idiopathic nephrotic syndrome in adults. Minimal change disease and (less commonly) immunoglobulin A (IgA) nephropathy cause ˜25% of cases of idiopathic nephrotic syndrome. Other conditions, such as membranoproliferative glomerulonephritis, are less common. FSGS accounts for ˜3.3% of new cases of end-stage renal disease. A large number of secondary causes of nephrotic syndrome have been identified ([Table 3]), with diabetes mellitus being the most common. According to Haraldsson et al. [9], the underlying pathophysiology of nephrotic syndrome is not completely clear. Although the more intuitive 'underfill' mechanism of edema from reduced oncotic pressure caused by marked proteinuria may be the primary mechanism in children with acute nephrotic syndrome, edema in adults may be caused by a more complex mechanism. According to Machuca et al. [10], massive proteinuria causes renal tubulointerstitial inflammation, with resulting increased sodium retention that overwhelms the physiologic mechanisms to eliminate edema. Patients may have an 'overfilled' or expanded plasma volume in addition to expanded interstitial fluid volume. This may be clinically important if over-rapid diuresis leads to acute renal failure from reduced glomerular blood flow, despite persistent edema. According to Koomans [11], common presenting symptoms may be nonspecific and include edema, anorexia, and malaise. Frothy urine (caused by a high concentration of protein in the urine) is a more specific presenting complaint. Fluid retention in NS (Nephrotic Syndrome) does not produce symptoms of heart failure. Shortness of breath in NS is most often related to pleural effusions or pulmonary embolism. Pulmonary edema almost never occurs in NS unless some organic disease of the heart is also present. According to Kashif et al. [12], heart failure is often the initial (incorrect) diagnosis – until the urine is examined for proteinuria. This is understandable; NS is uncommon and congestive cardiac failure is not. Classical signs may develop, including peripheral edema. Edema may obscure signs of muscle wasting. According to Caring for Australians with Renal Impairment (CARI) [13], nephrotic-range proteinuria is typically defined as greater than 3–3.5 g of protein in a 24-h urine collection; however, not all patients with this range of proteinuria have nephrotic syndrome. Although a urine dipstick proteinuria value of 3 + is a useful semiquantitative means of identifying nephrotic-range proteinuria, given the logistic difficulties of collecting a 24-h urine sample, the random urine protein/creatinine ratio is a more convenient quantitative measure. The numeric spot urine protein/creatinine ratio, in mg/mg, accurately estimates protein excretion in g/day/1.73 m 2 of body surface area; thus, a ratio of 3–3.5 represents nephrotic-range proteinuria. According to CARI guidelines [14], low serum albumin levels [<2.5 g/dl (25 g/l)] and severe hyperlipidemia are also typical features of nephrotic syndrome. In one study of patients with nephrotic syndrome, 53% had a total cholesterol level greater than 300 mg/dl (7.77 mmol/l) and 25% had a total cholesterol level greater than 400 mg/dl (10.36 mmol/l). According to Ruggenenti et al. [15], diagnostic evaluation depends on the typical clinical and laboratory features of nephrotic syndrome that are sufficient to establish the diagnosis of nephrotic syndrome. The diagnostic evaluation focuses on identification of an underlying cause and on the role of renal biopsy. According to Kodner [16], initial investigation should include assessment of history, physical examination, and a serum chemistry panel. Given the large number of potential causes of nephrotic syndrome and the relatively nonspecific aspect of therapy, the diagnostic evaluation should be guided by a clinical suspicion for specific disorders, rather than a broad or an unguided approach to ruling out multiple illnesses. According to National Collaborating Centre for Chronic Conditions (UK) [17], the sequence of investigations in [Table 4] is typical of those used to assess the patient's current clinical status and identify the underlying cause of the syndrome. Assessment of the patient's renal function is a key part of this; serum urea and creatinine should be measured and an estimated glomerular filtration rate should be calculated. According to Hull and Goldsmith [4], imaging studies are generally not useful for the assessment of patients with nephrotic syndrome. Renal ultrasonography may identify renal venous thrombosis if suggestive features, such as flank pain, hematuria, or acute renal failure, are present. According to Adu [18], renal biopsy is often recommended in patients with nephrotic syndrome to establish the pathologic subtype of the disease, to assess disease activity, or to confirm the diagnosis of diseases, such as amyloidosis or systemic lupus erythematosus. There are, however, no clear guidelines on when renal biopsy is indicated or whether it is needed in all patients with nephrotic syndrome. According to Sinha et al. [19], patients may experience significant morbidity from complications of the disease or its treatment including severe edema, infections, and thromboembolism, which often leads to frequent hospitalizations and utilization of health care services. Complications of nephrotic syndrome include venous thromboembolism caused by loss of clotting factors in the urine, infection caused by urinary loss of immunoglobulins, and acute renal failure. According to Mahmoodi et al. [20] and Wu et al. [21], infection is also a possible complication of nephrotic syndrome; however, this risk appears primarily in children and in patients who have relapses of nephrotic syndrome or who require longer-term corticosteroid therapy. Invasive bacterial infections, especially cellulitis, peritonitis, and sepsis, are the most common infections attributable to nephrotic syndrome. According to Koomans [11], acute renal failure is a rare, spontaneous complication of nephrotic syndrome. Although older individuals, children, and those with more severe edema and proteinuria are at the highest risk, there are many possible causes or contributing factors to acute renal failure in this setting. Excessive diuresis, therapeutic drug complications, sepsis, renal venous thrombosis, renal interstitial edema, and marked hypotension may cause or contribute toward acute renal failure. According to Charlesworth et al. [22], treatment is based on the nature of the underlying glomerular lesion, which emphasizes the necessity of establishing a tissue diagnosis by performing a renal biopsy. Irrespective of the cause, the most important part of the treatment is to remove (or treat) the underlying problem. In some glomerulonephritis patients, immunosuppression is indicated. Other treatments of underlying disorders may include prompt treatment of infections (e.g., staphylococcal endocarditis, malaria, syphilis, schistosomiasis), allergic desensitization (e.g., for poison oak or ivy and insect antigen exposures), and stopping drugs (e.g., gold, penicillamine). According to Jalanko [23], the main aim is to control edema and possible uremia, prevent and treat complications such as infections and thrombosis as well as provide adequate nutrition to ensure optimal growth of the child. In many cases, the ultimate curative therapy is kidney transplantation ([Table 5]). According to Goldsmith et al. [24], and Davison et al. [25], loop diuretics such as furosemide are usually used, but drug absorption may be affected by edema of the gut wall; thus, large doses of intravenous diuretics are often used for refractory cases. Common diuretics are mostly protein bound; hence, their activity may be affected by severe proteinuria once filtered across the glomerulus. Thiazide diuretics or potassium-sparing diuretics are often added in an attempt to improve the poor responses sometimes found with loop diuretics. They are synergistic for distal inhibition of sodium reabsorption. The use of intravenous albumin infusion is controversial. According to Burden and Tomson [26], most physicians will not use an albumin infusion unless hypotension and volume depletion are unequivocally present. It is rarely effective and can be harmful. Patients with very low albumin levels may not respond to diuretics and may require admission to receive intravenous albumin therapy. Intravenous albumin probably acts by increasing delivery of the diuretic to its site of action and by expanding the plasma volume. It is often used in hypotensive patients in whom conventional treatment is failing. According to MacHardy et al. [27], the current approach to treatment is based on several seminal studies; patient management (choice of drugs, doses, and duration) is known to be highly variable between physicians and care centers. A better understanding of the factors driving this variation will impact the design of future clinical trials evaluating optimal duration of steroid therapy to minimize relapses and toxicity. According to Baigent et al. [28], the severity of hyperlipidemia is proportional to the degree of proteinuria. Therefore, successful disease-specific treatment or antiproteinuria treatment usually leads to an improvement in the lipid profile. Dietary fat restriction exerts only a modest effect on hyperlipidemia in nephrotic patients. Statins (HMG CoA reductase inhibitors) are the most commonly used agents for the treatment of nephrotic hyperlipidemia. LDL-cholesterol can be reduced by 35–40% and triglycerides can be reduced by 15–30%. According to Kayali et al. [29], this is of particular relevance during remission of proteinuria, when the anticoagulant effect of a stable dose of warfarin decreases. An alternative approach is treatment with aspirin and dipyridamole, which may also be beneficial, given the associated cardiovascular risk. According to Glassock [30] and Singhal and Brimble [31], patients with clinically apparent thromboembolic disease should be given anticoagulant heparin, followed by warfarin. Treatment should be continued for the duration of the nephrotic syndrome (or at least until serum albumin increases above 25 g/l) unless the risks of anticoagulation become prohibitive. The optimal treatment of clinically silent thromboembolism is less clear. Asymptomatic pulmonary emboli should prompt full anticoagulation, and most clinicians would fully anticoagulate those with silent deep venous thrombosis. According to Gibson et al. [32], specific treatment of nephrotic syndrome depends on the cause of the disease. In MCD (minimal change disease), glucocorticosteroids, such as prednisone, are used. Children who develop relapse after successful use of prednisone or who do not respond to prednisone (i.e., those with steroid-resistant disease) may be treated with rituximab, an antibody against B cells. Rituximab has also been used in membranous nephropathy in adults, whereas in some forms of lupus nephritis, prednisone and cyclophosphamide are useful. According to Fervenza et al. [33], secondary amyloidosis with nephrotic syndrome may respond to anti-inflammatory treatment of the primary disease, but in membranous nephropathy, expectant management without immunosuppressants can be used for the first 6 months in patients at low risk for progression (i.e., in membranous nephropathy), expectant management without immunosuppressants can be used for the first 6 months in patients at low risk for progression (i.e., those with serum creatinine level <1.5 mg/dl). Patients with renal insufficiency (serum creatinine level > 1.5 mg/dl) are at greatest risk for the development of end-stage renal disease and should receive immunosuppressive therapy. According to De Carvalho et al. [34], corticosteroids in SLE (systemic lupus erythematosus) patients can also lead to an increase in triacylglycerol levels, which seems to be mediated by increased plasma insulin levels and lipid production by the liver and also by impaired lipid catabolism.
Table 1 Diagnostic criteria for nephrotic syndrome

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Table 2 Sequence of investigations for a patient presenting with nephrotic syndrome

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Table 3 Histologic patterns and features of primary nephrotic syndrome

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Table 4 Common secondary causes of nephrotic syndrome

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Table 5 CNS management of infants with severe proteinuria

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According to Kidney Disease: Improving Global Outcomes (KDIGO) Glomerulonephritis Work Group [35], steroids are the treatment of choice both for first presentation and for subsequent relapses of nephrotic syndrome. Steroid treatment is supported by evidence published in systematic reviews and a recent international clinical practice guideline. Clinical response to steroids is the most important predictor of clinical outcome and prognosis.

According to Gipson et al. [36], relapses of proteinuria are common in nephrotic syndrome and require multiple courses of steroid therapy. The risk of relapse is strongly linked to cessation of steroids (i.e., when steroids are stopped, the likelihood of a relapse increases). Therefore, the duration of steroid treatment is a key determinant of patient outcomes including treatment and prevention of relapses and also steroid toxicity. According to Du Buf-Vereijken et al. [37], in secondary nephrotic syndrome, such as that associated with diabetic nephropathy, angiotensin-converting enzyme inhibitors and/or angiotensin II receptor blockers are used widely. These may reduce proteinuria by reducing the systemic blood pressure, by reducing intraglomerular pressure, and also by a direct action on podocytes. According toHoerger et al. [38], the treatment of kidney damage may reverse or delay the progression of the disease. Kidney damage is treated by prescribing drugs: corticosteroids (prednisone), cyclophosphamide, and cyclosporine are used to induce remission in nephrotic syndrome. Diuretics are used to reduce edema. According to Whaley-Connell et al. [39], follow-up care in patients with nephrotic syndrome includes immunization, treatment of relapses of steroid-responsive nephrotic syndromes, monitoring for steroid toxicity, and monitoring of diuretic and angiotensin antagonist regimens. All children with nephrotic syndrome should receive immunization against pneumococcal infections. It is important to note that not all pneumococcal serotypes are included in the vaccines and that antibody levels may decrease during a relapse. According to Vogt and Avert [40], parental motivation and involvement is essential in the long-term management of these children. They should be provided information on the disease, its expected course, and the risk of complications. The following should be performed: urine examination for protein can be carried out at home using a dipstick, sulfosalicylic acid, or the boiling test. The examination should be performed every morning during a relapse, during intercurrent infections, or if there is even mild periorbital puffiness. The frequency of urine examination is reduced to once or twice a week during remission. It is important to detect relapse before the development of significant edema. According to Gulati et al. [41], patients should be advised to maintain a diary with the results of urine protein examination, the medications received, and intercurrent infections. Normal activity and school attendance should be ensured; the child should continue to participate in all activities and sports. As infections are an important cause of morbidity, patients should receive appropriate immunization and other measures for protection. According to Swierzewski [42], the outcome of NS varies and is largely dependent on the underlying cause. Some patients may achieve a spontaneous recovery without the need for any specific therapy, whereas others worsen despite aggressive, specific therapy. The condition may be acute and short-term or chronic and may not respond to treatment. The complications that occur can also affect the outcome. Some patients may eventually require dialysis and a kidney transplant. According to Nachman et al. [43], family physicians must be equipped to care for this unique patient population. Irrespective of the underlying etiology of the chronic kidney disease, the family physician can make a significant contribution toward slowing the progression of chronic kidney disease through strict blood pressure control, tight glycemic control, reduction in the degree of proteinuria, and smoking cessation. Early screening and treatment of these complication can prevent the development of further sequelae and should not be delayed until referral to nephrology.

  Conclusion Top

Nephrotic syndrome can present in diverse ways in multiple healthcare settings and has major complications. Investigation and management of the syndrome are made more challenging by the lack of a guiding evidence base, but strategies derived from expert consensus are available for its initial management. Large randomized trials in the management of the nephrotic syndrome, and in glomerular disease in general, are urgently needed to achieve further progress.

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Conflicts of interest

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  References Top

Bope ET, Kellerman RD, editors. Conn's current therapy. Philadelphia, PA: Saunders; 2013.  Back to cited text no. 1
Kari JA. Changing trends of histopathology in childhood nephritic syndrome in western Saudi Arabia. Saudi Med J 2002; 23:317–321.  Back to cited text no. 2
Domino FJ, editor. Five minute clinical consult. Philadelphia, PA: Lippincott Williams and Wilkins; 2013.  Back to cited text no. 3
Hull RP, Goldsmith DJ. Nephrotic syndrome in adults.BMJ 2008; 336: 1185–1189.  Back to cited text no. 4
Zacchia M, Trepiccione F, Morelli F, Pani A, Capasso G Nephrotic syndrome: new concepts in the pathophysiology of sodium retention. J Nephrol 2008; 21: 836-842.  Back to cited text no. 5
Kitiyakara C, Kopp JB, Eggers P. Trends in the epidemiology of focal segmental glomerulosclerosis. Semin Nephrol 2003; 23: 172–182.  Back to cited text no. 6
Cameron JS, Hicks J. The origins and development of the concept of a 'nephrotic syndrome'. Am J Nephrol 2002; 22: 240–247.  Back to cited text no. 7
Jayawardene SA, Scoble JE, Goldsmith DJ. Nephrotic syndrome: more than just oedema. Int J Clin Pract 2002; 56: 129–131.  Back to cited text no. 8
Haraldsson B, Nyström J, Deen WM. Properties of the glomerular barrier and mechanisms of proteinuria. Physiol Rev 2008; 88: 451–487.  Back to cited text no. 9
Machuca E, Benoit G, Antignac C. Genetics of nephrotic syndrome: connecting molecular genetics to podocyte physiology. Hum Mol Genet 2009; 18: R185–R194.  Back to cited text no. 10
Koomans HA. Pathophysiology of acute renal failure in idiopatic nephrotic syndrome. Nephrol Dial Transplant 2001; 16: 221–224.  Back to cited text no. 11
Kashif W, Siddiqi N, Dincer AP, Dincer HE, Hirsch S Proteinuria: how to evaluate an important finding. Cleve Clin J Med 2003; 70: 535–537, 541–544, 546–547.  Back to cited text no. 12
Leung YY, Szeto CC, Tam LS, Lam CW, Li EK, Wong KC, et al. Urine protein-to-creatinine ratio in an untimed urine collection is a reliable measure of proteinuria in lupus nephritis. Rheumatology (Oxford) 2007; 46: 649–652.  Back to cited text no. 13
Caring for Australians with Renal Impairment (CARI) The CARI guidelines. Urine protein as diagnostic test: testing for proteinuria. Nephrology (Carlton) 2004; 9 (Suppl 3): S3–S7.  Back to cited text no. 14
Ruggenenti P, Mosconi L, Vendramin G, Moriggi M, Remuzzi A, Sangalli F, Remuzzi G ACE inhibition improves glomerular size selectivity in patients with idiopathic membranous nephropathy and persistent nephrotic syndrome. Am J Kidney Dis 2000; 35: 381–391.  Back to cited text no. 15
Kodner C. Nephrotic syndrome in adults: diagnosis and management. Am Fam Physician 2009; 80: 1129–1134  Back to cited text no. 16
National Collaborating Centre for Chronic Conditions (UK). Chronic kidney disease: National Clinical Guideline for early identification and management in adults in primary and secondary care. London: Royal College of Physicians; 2008.  Back to cited text no. 17
Adu D. The nephrotic syndrome: does renal biopsy affect management? Nephrol Dial Transplant 1996; 11: 12–14.  Back to cited text no. 18
Sinha A, Hari P, Sharma PK, Gulati A, Kalaivani M, Mantan M, et al. Disease course in steroid sensitive nephrotic syndrome. Indian Pediatr 2012; 49: 881–887.  Back to cited text no. 19
Mahmoodi BK, ten Kate MK, Waanders F, Veeger NJ, Brouwer JL, Vogt L, et al. High absolute risks and predictors of venous and arterial thromboembolic events in patients with nephrotic syndrome: results from a large retrospective cohort study. Circulation 2008; 117: 224–230.  Back to cited text no. 20
Wu HM, Tang JL, Sha ZH, Cao L, Li YP. Interventions for preventing infection in nephrotic syndrome. Cochrane Database Syst Rev 2004; 2:CD003964.  Back to cited text no. 21
Charlesworth JA, Gracey DM, Pussell BA Adult nephrotic syndrome: non-specific strategies for treatment. Nephrology (Carlton) 2008; 13: 45–50.  Back to cited text no. 22
Jalanko H. Congenital nephrotic syndrome. Pediatr Nephrol 2009; 24:2121–2128.  Back to cited text no. 23
Goldsmith DJ, Jayawardene S, Ackland P, editors. ABC of kidney disease. Oxford: Blackwell Publishing; 2007.  Back to cited text no. 24
Davison AMA, Cameron JS, Grunfeld JP, Ponticelli C, Ypersele CV, Ritz E, et al., editors. Oxford textbook of clinical nephrology. 3rd ed. Oxford: Oxford University Press, 2005.  Back to cited text no. 25
Burden R, Tomson C. Identification, management and referral of adults with chronic kidney disease: concise guidelines. Clin Med 2005; 5: 635–642.  Back to cited text no. 26
MacHardy N, Miles PV, Massengill SF, Smoyer WE, Mahan JD, Greenbaum L, et al. Management patterns of childhood-onset nephrotic syndrome. Pediatr Nephrol 2009; 24: 2193–2201.  Back to cited text no. 27
Baigent C, Landray MJ, Reith C, Emberson J, Wheeler DC, Tomson C, et al. SHARP Investigators The effects of lowering LDL cholesterol with simvastatin plus ezetimibe in patients with chronic kidney disease (Study of Heart and Renal Protection): a randomised placebo-controlled trial. Lancet 2011; 377: 2181–2192.  Back to cited text no. 28
Kayali F, Najjar R, Aswad F, Matta F, Stein PD. Venous thromboembolism in patients hospitalized with nephrotic syndrome. Am J Med 2008; 121: 226–230.  Back to cited text no. 29
Glassock RJ. Prophylactic anticoagulation in nephrotic syndrome: a clinical conundrum. J Am Soc Nephrol 2007; 18: 2221–2225.  Back to cited text no. 30
Singhal R, Brimble KS. Thromboembolic complications in the nephrotic syndrome: pathophysiology and clinical management. Thromb Res 2006; 118: 397–407.  Back to cited text no. 31
Gibson KL, Gipson DS, Massengill SA, Dooley MA, Primack WA, Ferris MA, Hogan SL Predictors of relapse and end stage kidney disease in proliferative lupus nephritis: focus on children, adolescents, and young adults. Clin J Am Soc Nephrol 2009; 4: 1962–1967.  Back to cited text no. 32
Fervenza FC, Abraham RS, Erickson SB, Irazabal MV, Eirin A, Specks U, et al. Mayo Nephrology Collaborative Group Rituximab therapy in idiopathic membranous nephropathy: a 2-year study. Clin J Am Soc Nephrol 2010; 5: 2188–2198.  Back to cited text no. 33
De Carvalho JF, Borba EF, Viana VS, Bueno C, Leon EP, Bonfa E. Antilipoprotein lipase antibodies: a new player in the complex atherosclerotic process in systemic lupus erythematosus? Arthritis Rheum 2004; 50:3610–3615.  Back to cited text no. 34
Kidney Disease: Improving Global Outcomes (KDIGO) Glomerulonephritis Work Group. KDIGO clinical practice guideline for glomerulonephritis. Kidney Int Suppl 2012; 2:139–274.  Back to cited text no. 35
Gipson DS, Massengill SF, Yao L, Nagaraj S, Smoyer WE, Mahan JD, et al. Management of childhood onset nephrotic syndrome. Pediatrics 2009; 124: 747–757.  Back to cited text no. 36
Du Buf-Vereijken PW, Branten AJ, Wetzels JF. Idiopathic membranous nephropathy: outline and rationale of a treatment strategy. Am J Kidney Dis 2005; 46: 1012–1029.  Back to cited text no. 37
Hoerger TJ, Wittenborn JS, Segel JE, Burrows NR, Imai K, Eggers P, et al. A health policy model of CKD: 2. The cost-effectiveness of microalbuminuria screening. Am J Kidney Dis 2010; 55: 463–473.  Back to cited text no. 38
Whaley-Connell AT, Sowers JR, Stevens LA, McFarlane SI, Shlipak MG, Norris KC, et al. Kidney Early Evaluation Program Investigators CKD in the United States: Kidney Early Evaluation Program (KEEP) and National Health and Nutrition Examination Survey (NHANES) 1999–2004. Am J Kidney Dis 2008; 51 (Suppl 2): S13–S20.  Back to cited text no. 39
Vogt AB, Avner ED. Nephrotic syndrome. In: Kliegman RM, Behrman RE, Jenson HB, Stanton BF, editors. Nelson textbook of pediatrics. 18th ed. Philadelphia, PA: WB Saunders; 2007. 2190–50.  Back to cited text no. 40
Gulati S, Sharma RK, Gulati K, Singh U, Srivastava A. Longitudinal follow-up of bone mineral density in children with idiopathic nephrotic syndrome. Nephrol Dial Transplant 2005; 20:1598–1603.  Back to cited text no. 41
Lane JC. Kaskel FJ. Pediatric Nephrotic Syndrome: From the Simple to the Complex. Seminars in Nephrology 2009;29(4):389-398.  Back to cited text no. 42
Nachman PH, Jennette JC, Falk RJ. Primary glomerular disease [chapter 30]. In: Brenner BM, editor. Brenner and Rector's the kidney. 8th ed. Philadelphia, PA: Saunders Elsevier; 2007.  Back to cited text no. 43


  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]


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