Claire Kleinknecht

Extramembranous glomerulonephritis inchildren: Report of 50 cases

Pathologic and clinical data concerning 50 children with extramembranous glomerulonephritis (EMGN) are reported. This type of glomerular lesion is characterized by thickening of the capillary walls, due to subepithelial deposits without endocapillary proliferation. EMGN occurred in all age groups including infancy. It was often latent and discovered by routine urinalysis. Nephrotic syndrome and hematuria were frequent but not constant. In no instance could a specific etiology be demonstrated. Corticosteroids as well as immunosuppressive drugs seemed ineffective. Remissions often occurred while patients received no treatment. Patients were followed for one to ten years. Twenty-six children had complete remissions, 17 of them without subsequent relapse. Twenty-four patients had persistent proteinuria. The only five patients who developed chronic renal failure presented with persistent biochemical changes of the nephrotic syndrome. EMGN is not an uncommon nephropathy in children, but seems to have a more benign course in children than in the older age groups hitherto reported.

Membranous glomerulonephritis with extra-renal disorders in children.

Thirty of 85 children with membranous glomerulonephritis (MGN) had associated extraglomerular disorders. The relation of these associations to membranous glomerulonephritis (MGN) is discussed. The causal relationship of acute hepatitis (5 cases), persistent hepatitis B antigenemia (6 cases), systemic lupus erythematosus (2 cases) and syphilis (1 case) may be ascertained; in similar conditions a definite antigen (Ag) has been found in MGN deposits. The association with SS or SA hemoglobinopathy (3 cases) ans with a preceding streptococcal infection (4 cases) raises the possible responsibility of renal tubular epithelium (RTE) Ag and of a streptococcal Ag. D-penicillamine therapy (1 case) is a well-known cause of MGN although the acting Ag remains unknown. Four children had serum sickness-like symptoms, two had hematologic disorders and two had proximal tubular dysfunction, one of them with proven anti-tubular and anti-alveolar basement membrane antibodies. A decrease in plasma C4, Clq, and factor B with normal C3 was frequently observed. The multiple Ag previously described as causative of MGN are recalled. The prevalent incidence of HBsAg is stressed, and the necessity for further investigations in patients with MGN in order to find an underlying disease is emphasized.

Acidosis prevents growth hormone-induced growth in experimental uremia

The effects of 2 weeks of a daily injection (2 IU/day) of recombinant human growth hormone (GH) were studied in young (60-g) growing rats in two experiments. Experiment 1 was performed in uremic animals (mean plasma creatinine 65–71 μmol/l) who were either acidotic (mean bicarbonate 11.5 mmol/l) or had acidosis corrected (mean bicarbonate 26 mmol/l) by addition of sodium bicarbonate to the diet. Experiment 2 used rats with normal renal function (plasma creatinine 25 μmol/l) who were either non-acidotic but restricted to the dietary intake of uremic rats or rendered acidotic by ammonium chloride. GH induced an increase in body weight and length in nonacidotic uremic (+33% and +41%) and in non-acidotic food-restricted (+13% and +42%) rats, associated with an increased rate of protein synthesis and little change in plasma insulin-like growth factor 1 (IGF 1). In both acidotic rat groups, GH altered none of the parameters studied. Thus: (1) the presence of severe metabolic acidosis blunts the response to GH in uremic and non-uremic rats and (2) the increment of growth rate does not depend on a rise in plasma IGF 1.

Coexistence of antenatal, infantile, and juvenile nephrotic syndrome in a single family

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