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Background: Children with post-infectious glomerulonephritis (PIGN) rapidly recover and have excellent long-term outcomes. After encountering several overweight/obese children with persistent urinary abnormalities during recovery from PIGN, we conducted this retrospective study to determine if overweight/obese status prolonged time to resolution of renal abnormalities after PIGN., Methods: Records of 20 children with PSGN evaluated between 1/98 and 12/05 were abstracted for demographics, clinical and laboratory data. Primary outcome measures were time to resolution of hypertension, proteinuria, microhematuria, and low complement C3. The effect of overweight/obese status on outcomes was determined using Kaplan Meier Survival and the log-rank test., Results: The median age was 8 years; 30% were overweight/obese. At presentation, 17 (85%) were hypertensive, 10 (50%) had impaired glomerular filtration (GFR), and 18 (90%) had proteinuria. At last follow-up (median 2.8 months) 12% had hypertension, 55% had microhematuria, 5% had proteinuria but none had low GFR. Median time to normalize was: 30 days (GFR), 45 days (blood pressure), 6 weeks (C3) and 6 months (microhematuria). Log rank test showed that proteinuria-, hypertension-, and hematuria-free survival were all lower in children who were overweight/obese although none of the differences were statistically significant. Time to normalization of C3 was shorter in obese/ overweight children., Conclusion: In conclusion, overweight/obese children appear to have greater residual renal injury after PIGN. The earlier C3 normalization in overweight/ obese children may indicate that the adverse effect of weight on recovery is from hemodynamic rather than inflammatory factors. Close follow-up of overweight/obese children who develop PIGN is warranted to ensure optimal long-term outcomes.

This study investigated predictors of renal survival in children with Henoch-Schönlein purpura glomerulonephritis. Records of patients with Henoch-Schönlein purpura glomerulonephritis evaluated at our center, from 1953-1990, were reviewed. Data were abstracted from records of patients seen within 5 years. Others were mailed a questionnaire or contacted by telephone. Primary outcome measures were renal survival and presence of urinary abnormalities or hypertension. Of the 65 eligible patients with Henoch Schönlein purpura glomerulonephritis, follow-up data was obtainable for 81.5%. The median follow-up was 20 years. At last follow-up, 66% of patients had normal renal function and urinalyses, and 21% had progressed to end-stage renal disease. The only factor associated with the development of end-stage renal disease was the use of cytotoxic agents. There are no features at initial presentation that identify children at risk of disease progression. Close follow-up of all children with Henoch Schönlein purpura glomerulonephritis is warranted.

Patients with chronic proteinuric nephropathies are at high risk of developing progressive renal insufficiency. There are limited controlled data on the efficacy of potentially toxic immunosuppressive therapies for many of these diseases such as immunoglobulin A nephropathy and idiopathic membranoproliferative glomerulonephritis. This limitation has not deterred healthcare providers from using such agents based on anecdotal experience. We report our experience taking care of three children with heavy proteinuria from chronic glomerular diseases. All were treated with a combination of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers without concomitant immunosuppression. All went into complete remission soon after starting therapy, allowing corticosteroid avoidance. The purpose of this report is to make healthcare professionals more aware of the potential success that can be achieved with this relatively nontoxic drug regimen. Larger controlled clinical trials using this strategy are needed to better evaluate the efficacy and safety of this approach in children with glomerular diseases.

Primary anti-phospholipid syndrome (APS) is perceived to be an uncommon disorder, infrequently recognized as a cause of renal disease in childhood. While renal involvement in APS classically manifests as thrombotic events, other renal diseases associated with APS have been reported in adults, including membranous nephropathy and minimal change disease. We report our experience of caring for a child who presented with acute anuric renal failure due to anti-neutrophilic cytoplasmic antibody-negative rapidly progressive glomerulonephritis (RPGN), with concomitant thrombotic microangiopathy (TMA). Recognition of the APS as a cause of the patient's TMA facilitated institution of anticoagulation. Our patient's renal failure did not improve and the patient remained dependent on dialysis until he was successfully transplanted. The purpose of our report is to make health-care professionals aware of the previously unreported association of pauci-immune RPGN and APS in children; early recognition of APS will allow initiation of anticoagulation to prevent recurrent thromboses and enable successful transplantation.

We describe our experience managing a 16-year-old girl with systemic lupus erythematosus (SLE) who presented concomitantly with rapidly progressive glomerulonephritis (RPGN) and a thrombotic microangiopathic hemolytic anemia (TMAHA). Her renal biopsy showed evidence of diffuse proliferative glomerulonephritis without glomerular microthrombi. The patient was treated with a combination of intravenous corticosteroids and cyclophosphamide, as well as plasmapheresis, with an excellent response resulting in complete disease remission. The purpose of our report is to make health professionals more aware of TMAHA as a complication of SLE, since the occurrence of TMAHA may confuse the clinical picture, and since its treatment with plasmapheresis is life saving, if performed early. [ABSTRACT FROM AUTHOR]