Determination of prevalence of asymptomatic proteinuria and haematuria in 5-15 year aged school children in southern India

Background: Chronic renal diseases remain major cause of morbidity and mortality in young children. Although idiopathic nephrotic syndrome takes on chronic course other histopathological variants can lead to rapid progression of disease. Proteinuria in children can be physiological. Hematuria in children is always should be investigated. Persistent proteinuria in children should be investigated for any significant progressive renal disease after excluding orthostatic proteinuria. Although many countries adopt high risk screening in pediatric age group many eastern countries advocate school screening for asymptomatic proteinuria and hematuria using dipstick urine screening.Methods: A 6 month cross sectional study of asymptomatic children aged 5-15 years in metropolitan school for dipstick urine analysis for proteinuria and hematuria.Results: The ratio of male and female children in the study is 1.2:1 (total-1999, male-1056, and female-934). Age group ranged from 5 to 15 with mean 12.13 and standard deviation (SD)-2.46. Maximum number of students in the study are above 10 years of age. Children with isolated asymptomatic proteinuria have significant differences due to their sex (p value-0.005) and hematuria (p value-0.007). Prevalence of asymptomatic proteinuria is 9.8% and hematuria is 1.05%. Prevalence of persistent proteinuria is 1.35%.Conclusions: Prevalence of asymptomatic proteinuria and hematuria can be determined using dipstick urine analysis in school children. Mass screening is cost effective and feasible only if persistent cases of proteinuria are followed up, ruling out orthostatic proteinuria. Although study is feasible, it is cumbersome. High risk screening is the best cost effective method.

Membranous nephropathy

Membranous nephropathy (MN) is the most common cause of nephrotic syndrome in Caucasians adults. It may also present with asymptomatic proteinuria. Its defining feature is the presence of subepithelial immune deposits, localized between the podocyte and the glomerular basement membrane. Aetiology—primary MN (80% of cases) is caused in most cases by antibodies against the M-type phospholipase A2 receptor (PLA2R). Secondary MN occurs as a consequence of drugs, malignancy, or autoimmune disease. Prognosis—the clinical course of primary MN is variable: spontaneous complete remission of proteinuria occurs in 20 to 30% and progressive kidney failure develops in 20 to 40% over 5 to 15 years. Patients with gross proteinuria (>8 g/day) are at high risk of progression, as are those with a high and rising anti-PLA2R antibody level. Management—patients at low risk of progression have an excellent long-term prognosis and should be treated conservatively without immunosuppression. Patients at medium and high risk for progression benefit from immunosuppression in addition to conservative treatment. Corticosteroid monotherapy is ineffective in primary MN and should not be used. Standard treatment regimens include corticosteroids with alkylating agents (chlorambucil, cyclophosphamide), corticosteroids with mycophenolate mofetil, and calcineurin inhibitors (ciclosporin, tacrolimus). Early experience with rituximab has given some promising results.

Atypical Plasmacytic Proliferation in a Case of C3 Glomerulopathy

An 11-year-old Hispanic female underwent evaluation of asymptomatic proteinuria and hematuria. The patient denied fever, edema, and gross hematuria. Urinalysis showed mild proteinuria, and a urine microscopic examination revealed red blood cells. Screening tests for glomerulonephritis revealed a low C3 and negative ANA, ASO, DNAse-B, and ANCA. Histological examination of a renal biopsy specimen showed glomeruli with endocapillary proliferation, a predominant C3 deposition in the capillary loops by immunofluorescence, and electron dense deposits in the mesangium, paramesangium, and capillary walls by electron microscopy consistent with a diagnosis of C3 glomerulopathy. An interstitial plasmacytosis was also present with focal clustering of plasma cells, which were found to be kappa light chain restricted by in situ hybridization suggestive of a clonal proliferation. One can speculate that these plasma cells may be directly responsible for the renal pathology that was seen.