Acute Poststreptococcal Glomerulonephritis: The Most Common Acute Glomerulonephritis

Abstract

On the basis of strong research evidence, the prevalence of poststreptococcal glomerulonephritis (PSGN) is decreasing worldwide, although it still remains the leading cause of glomerulonephritis in children. The overall decrease in prevalence of PSGN has been mainly driven by a significant decrease in pyoderma seen in the last half-century, such that postpharyngitic PSGN is most commonly seen in developed nations. On the basis of primarily consensus because of a lack of relevant clinical studies, the latency period between streptococcal infection and the development of nephritis is a hallmark of PSGN, with this period lasting 1 to 2 weeks with pharyngeal infections or 2 to 6 weeks with skin infections. Concurrent infectious and nephritis symptoms should elicit further suspicion of other causes of glomerulonephritis. On the basis of expert opinion, PSGN is one of a handful of nephritic disorders with hypocomplementemia (low C3 level). The decrease in C3 is found in more than 90% of PSGN cases and is typically seen earlier than an increase in antistreptolysin O titers. Measuring C3 and C4 may also be helpful in the evaluation of other causes of acute nephritis. On the basis of primarily consensus because of a lack of relevantclinical studies, the main sequelae of PSGN (hypertension, edema,gross hematuria, and impaired renal function) are greatest in thefirst 7 to 10 days of disease. Therefore, this period requires themost vigilance for adverse effects. On the basis of some research evidence and consensus, the most effective treatment of hypertension and edema in PSGN is loop or thiazide diuretics, which may also address hyperkalemia. Angiotensin-converting enzyme inhibitors or angiotensin receptor blockers may be effective in hypertension control but carry the risk of hyperkalemia and temporarily impairing recovery of renal function. On the basis of some research evidence and consensus, the prognosis for PSGN, even long term, is good. Despite being the most prevalent of the childhood glomerulonephritides, it often does not cause chronic kidney disease, but persistent microscopic hematuria and proteinuria may be seen in less than 10% of patients.

Atypical presentation of acute post-infectious glomerulonephritis in patients with sickle cell disease: report of two cases

“…In recent years, the profile of APIGN has been changing, and the incidence of the disease in patients with other comorbidities such as diabetes, alcoholism and elderly patients has increased. In such situations, several other types of microorganisms may be associated with the disease, there may be atypical clinical manifestations (such as nephrotic proteinuria and/or nephrotic syndrome), different histological findings such as predominance of IgA to immunofluorescence, as well as a higher chance of evolution to chronic kidney disease [24][25][26].…”

Post-Infectious Acute Glomerulonephritis in Child: Epidemiological, Clinical and Evolutionary Aspects in Gabriel Touré Teaching Hospital in Mali

“…In Nigeria, McGilUgwu GI [19] suspected streptococcal infection in 35%. VanDeVoorde RG [20], assumed that proper management of infections has decreased this form of APIGN worldwide in general. Two of our patients had pneumonia in which we could neither find the germ nor associate it with APIGN.…”

Protracted Clinical Course of Postinfectious Glomerulonephritis in a Previously Healthy Child

“…Low plasma complement factor C3c level is indicative but not pathognomonic for PIGN since MPGN and lupus nephritis may also be associated with hypocomplementaemia. The boy was negative for anti-nuclear and ANCA screening and had normal levels of complement C4 [ 3 ]. A renal biopsy, although rarely indicated in PIGN, can be used to rule out other diagnoses.…”

“…PIGN in children is generally a self-limiting disease with excellent prognosis [ 2 ]. A small fraction of patients have persistent proteinuria and eventually progressive loss of kidney function leading to end-stage renal failure [ 3 , 4 ]. We herein describe a case of PIGN with protracted course in a previously healthy child.…”