Rapidly progressive glomerulonephritis (RPGN), characterized by a rapid development of nephritis with loss of kidney function in days or weeks, is typically associated histologically, with crescents in most glomeruli; and is a challenging problem, particularly in low resource settings. RPGN is a diagnostic and therapeutic emergency requiring prompt evaluation and treatment to prevent poor outcomes. Histopathologically, RPGN consists of four major categories, anti-glomerular basement membrane (GBM) disease, immune complex mediated, pauci-immune disorders and idiopathic /overlap disorders. Clinical manifestations include gross hematuria, proteinuria, oliguria, hypertension and edema. Diagnostic evaluation, including renal function tests, electrolytes, urinalysis/microscopy and serology including (anti GBM antibody, antineutrophil cytoplasmic antibody (ANCA)) starts simultaneously with management. An urgent renal biopsy is required to allow specific pathologic diagnosis as well as to assess disease activity and chronicity to guide specific treatment. The current guidelines for management of pediatric RPGN are adopted from adult experience and consist of induction and maintenance therapy. Aggressive combination immunosuppression has markedly improved outcomes, however, nephrotic syndrome, severe acute kidney injury requiring dialysis, presence of fibrous crescents and chronicity are predictors of poor renal survival. RPGN associated post infectious glomerulonephritis (PIGN) usually has good prognosis in children without immunosuppression whereas immune-complex-mediated GN and lupus nephritis (LN) are associated with poor prognosis with  development of end stage kidney disease (ESKD) in more than 50% and 30% respectively. Given the need for prompt diagnosis and urgent treatment to avoid devastating outcomes, we conducted a review of the latest evidence in RPGN management to help formulate clinical practice guidance for children in our setting.Information sources and search strategy: The search strategy was performed in the digital databases of PubMed, Cochrane Library, google scholar, from their inception dates to December 2020. Three investigators independently performed a systematic search using the following search terms “Rapidly progressive glomerulonephritis” “children” “crescentic glomerulonephritis” “management” at the same time, backtracking search for references of related literature. doi: https://doi.org/10.12669/pjms.38.ICON-2022.5774 How to cite this:Moorani KN, Aziz M, Amanullah F. Rapidly progressive glomerulonephritis in children. Pak J Med Sci. 2022;38(2):417-425.   doi: https://doi.org/10.12669/pjms.38.ICON-2022.5774 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Atherosclerosis is a cardiovascular disease that involves vessels through the development of fatty streaks and plaques. Plant-based compounds can help treat or prevent atherosclerosis by affecting various factors that are involved in the disease. The present review discusses our current knowledge of the major cellular and molecular mechanisms of phytotherapeutics for the treatment of atherosclerosis. Numerous studies have evaluated the antiatherosclerotic activity of phytoconstituents to provide preliminary evidence of efficacy, but only a few studies have delineated the underlying molecular mechanisms. Plant-derived phytotherapeutics primarily targets abnormal levels of lipoproteins, endothelial dysfunction, smooth muscle cell migration, foam cell development, and atheromatous plaque formation. Nonetheless, the principal mechanisms that are responsible for their therapeutic actions remain unclear. Further pharmacological studies are needed to elucidate the underlying molecular mechanisms of the antiatherosclerotic response to these phytoconstituents.

Objective: To screen asymptomatic siblings of steroid-resistant nephrotic syndrome patients for proteinuria using the urinary dipstick method to determine the involvement of siblings in the familial and likely genetic cause of the steroid-resistant nephrotic syndrome. Methods: This cross-sectional study was performed at the outpatient department of Sindh Institute of Urology and Transplantation (SIUT) from May to July 2021. Results: Out of 104 patients with steroid-resistant nephrotic syndrome, siblings of 66 patients were enrolled. Mean age of primary patients with steroid resistant nephrotic syndrome was 8.7±4.3 years. Most common histopathological diagnosis was focal segmental glomerulosclerosis in 25 (37.9%) children followed by minimal change disease in 17(25.8%) of them. The majority, 48 (72.7%) patients were on immunosuppressive treatment, while 4 (6.1%) had progressed to chronic kidney disease (CKD). A total of 178 siblings were recruited in the study. There were 99(55.6%) boys and 79(44.4%) girls. Their mean age was 10.67±6.2 years. Consanguinity was high in our study population i.e. 56(84%) families. Positive proteinuria on dipstick was detected in only 5(7.5%) enrolled SRNS families. One family refused further testing. Two of the five affected siblings had nephrotic range proteinuria. Renal biopsy of one of them showed membranous nephropathy while the second showed mesangiocapillary glomerulonephritis. Both had normal renal functions. Conclusion: The frequency of proteinuria in asymptomatic siblings of children with steroid-resistant syndrome is low in our population despite a high prevalence of consanguineous marriages. Hence, familial involvement of nephrotic syndrome is low and further genetic testing for monogenic causes is required in steroid-resistant nephrotic syndrome cases. Keywords: steroid-resistant, nephrotic, syndrome, proteinuria.

The pharmacokinetic properties of difloxacin were investigated following intravenous, intramuscular and oral administration of 10 mg/kg body weight, in non-infected and experimentally mycoplasma infected chickens. Serum concentrations of difloxacin were assayed microbialogically after intravenous, intramuscular and oral administrations. difl-oxacin residues were detected in chicken tissues following repeated oral administrations in non-infected and infected chickens. Following a single intravenous injection, the serum difloxacin level was best approximated to follow a two-compartment open model. The elimination half-life (t0.5) was 4.58 + 0.008 h. The volume of distribution at steady-state (Vdss) was 2.12 + 0.07 L/kg and the mean residence time (MRT) was 3.91 + 0.07 h.