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Biomedical subjects

A V Moorthy

Publications and source records attributed to A V Moorthy.

43 records · Page 3Linked to original sources
PubMed1976

Nephrotic syndrome in Hodgkin's disease. Evidence for pathogenesis alternative to immune complex deposition.

The nephrotic syndrome has been reported to occur in patients with Hodgkin's disease even in the absence of amyloidosis, tumor infiltration of renal vein thrombosis. Three patients are presented with Hodgkin's disease and the nephrotic syndrome whose renal biopsy specimens studied with light, immunofluorescence and electron microscopy were compatible with "lipoid nephrosis" (minimal change disease). A review of the literature reveals 35 patients with Hodgkin's disease and the nephrotic syndrome. Renal tissue was available for examination in only 27 patients. The majority of patients apparently had glomerular alterations consistent with lipoid nephrosis. The nephrotic syndrome in most of these patients remitted with a variety of methods of therapy (including excision, irradiation, prednisone and cyclophosphamide) and tended to relapse with a recurrence of Hodgkin's disease. In three-fourths of the patients with Hodgkin's disease and the nephrotic syndrome, the Hodgkin's disease was of a mixed cellularity type. The etiology of lipoid nephrosis, although unclear, may be a consequence of altered lymphocyte function. Hodgkin's disease is a malignancy involving T lymphocytes, and the nephrotic syndrome occurring in the course of Hodgkin's disease may be a result of an adverse effect of glomeruli by products of tumor lymphocytes rather than of glomerular deposition of immune complexes.

Adolescent↗
PubMed1976

Association of crescentic glomerulonephritis with membranous glomerulonephropathy: a report of three cases.

Association of membranous glomerulonephropathy with crescentic glomerulonephritis is apparently extremely rare. We report three patients who had this combination. One patient had biopsy-proven membranous glomerulonephropathy thirteen months prior to sudden and rapid decline in renal function necessitating hemodialysis. A repeat renal biopsy showed a superimposed crescentic nephritis and antiglomerular (GBM) antibodies were demonstrable in the serum. A second patient had proteinuria of unknown duration and then developed renal failure. Renal biopsy showed crescentic nephritis with a fine granular glomerular immunofluorescence for IgG typical of membranous glomerulonephropathy. Anti-GBM antibodies were present in this patient's serum. The third patient presented with acute renal failure of moderate severity. A renal biopsy revealed crescentic nephritis, granular deposits of immunoglobulins, and epimembranous electron-dense deposits typical of membranous glomerulonephropathy. Although his creatinine clearance improved spontaneously, nephrotic syndrome has persisted and a repeat renal biopsy showed a progression of the membranous glomerulonephropathy with the disappearance of the crescentic lesions. The reason for this peculiar association of membranous glomerulonephropathy and crescentic glomerulonephritis is unclear. It is possible that deposition of immune-complexes along glomerular basement membrane may render the glomerulus more susceptible to additional injury from a variety of other agents. Alternatively, depostis formed in one disease could initiate release of normal or altered basement membrane material and lead to formation of anti-GBM antibodies and subsequent development.

Adult↗
PubMed1975

Platelet function in dialyzed and non-dialyzed patients with chronic renal failure.

Platelet function studies were performed on healthy volunteers, patients with stable chronic renal failure, hospital dialysis patients and home dialysis patients. In the non-dialyzed patients with chronic renal failure, there was inverse exponential relationship between serum creatinine and platelet adhesiveness indicating progressive impairment of platelet adhesiveness with creatinines in excess of 6 mg/100 ml. In the dialysis population there was an inverse linear relationship between platelet adhesiveness and pre-dialysis creatinine values. Platelet aggregation by ADP was normal in chronic renal failure patients with serum creatinines less than 6 mg/100 ml but was impaired in others. Both groups of dialysis patients also had impaired platelet aggregation but improvement appears obtainable by home dialysis. The results suggest that in chronic renal failure, platelet function is normal until serum creatinine exceeds 6 mg/100 ml and thereafter progressively deteriorates. Improvement is not obtained by 12 m2 hours of hospital dialysis but is by 18 m2 hours per week of home dialysis. Platelet function studies may be of value in assessing the adequacy of dialysis.

Creatinine↗
PubMedDate not supplied

A comparison of plasma and muscle carnitine levels in patients on peritoneal or hemodialysis for chronic renal failure.

We studied plasma, dialysate, and muscle carnitine levels in patients with stable chronic renal failure on hemodialysis, and intermittent peritoneal, or continuous ambulatory peritoneal dialysis (CAPD). In patients on hemodialysis, plasma carnitine levels fell from 46.2 +/- 4.5 mumol/l (mean +/- SEM) to 18.8 +/- 2.7 mumol/l immediately after the procedure (p less than 0.001). Depletion of muscle carnitine was found after hemodialysis (1,518 +/- 273 nmol/g wet weight of tissue) compared to normal levels of 5,230.5 +/- 142.7 nmol/g tissue (p less than 0.01). However, the plasma and muscle carnitine levels remained in the normal range in patients on intermittent peritoneal dialysis and CAPD. We postulate that the rapid decline in plasma levels of carnitine caused by hemodialysis initiates unilateral transport of the compound from muscle to the plasma, thus depleting the skeletal muscle stores of carnitine.

Carnitine↗