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Biomedical subjects

A V Moorthy

Publications and source records attributed to A V Moorthy.

At least 19 recordsLinked to original sources
PubMed1997

End-stage renal disease (ESRD) in patients with eating disorders.

We report on the development of end-stage renal disease in four young women with long duration of eating disorders. No other reason for end-stage renal disease could be identified in these patients. Long standing hypokalemia was noted in all. Renal ultrasonography in three patients showed small kidneys with increased cortical echogenicity and multiple small bilateral cysts. A renal biopsy in one showed chronic tubulo-interstitial disease and non-specific glomerulosclerosis consistent with hypokalemic nephropathy. The development of end-stage renal disease is yet another medical complication to be considered in patients with long-standing eating disorder. Chronic hypokalemia may play a role in the pathogenesis of renal disease in this setting.

Adult↗
PubMed1987

Chronic renal failure and XY gonadal dysgenesis: "Frasier" syndrome--a commentary on reported cases.

The development of chronic renal failure because of parenchymatous renal disease in patients in 46,XY gonadal dysgenesis was noted initially by Drash et al [J Pediatr 76:585-593, 1970]. However, we think that some of the cases reported as examples of the Drash syndrome are a different disorder. In this paper, we review six previously reported patients with streak gonads, pseudohermaphroditism, and renal failure. In several of these patients the diagnosis was established only after a successful kidney transplantation during evaluation for primary amenorrhea. Gonadoblastoma arising from the streak gonad was noted in five of the six patients. "Frasier" syndrome would be a suitable term to denote this association after Frasier et al, who described two patients in 1964. We recommend evaluation of the gonads in prepubertal girls with end-stage renal disease at risk for this syndrome.

Adult↗
PubMed1986

Procainamide pharmacokinetics in patients on continuous ambulatory peritoneal dialysis.

The pharmacokinetics of procainamide in patients on continuous ambulatory peritoneal dialysis have been studied. A mean peak plasma concentration of 3.2 +/- 0.6 microgram/ml was achieved about 2 h after a single 500-mg oral procainamide hydrochloride dose. The procainamide elimination half-life ranged from 6.1 to 15.3 h. Apparent oral clearance, 183.7 +/- 63.2 ml/min, was less than half that observed in healthy adults suggesting markedly reduced dosage requirements. Continuous ambulatory dialysis patients exhibit similar procainamide pharmacokinetic parameters as do end stage renal disease patients, most notably a prolonged elimination half-life and reduced oral clearance.

Acecainide↗
PubMed1986

Changing patterns and outcome of acute renal failure requiring hemodialysis.

To identify factors that may explain the persistently high mortality of acute renal failure (ARF), we compared the cause, clinical course, and outcome of 55 consecutive patients with ARF who underwent hemodialysis (HD) from 1962 to 1969 with 46 similar patients from 1979 to 1981 at the same medical center. We noted an overall increase in mortality from 54.5% to 71.7%. There was an increase in the number of elderly patients developing ARF, but age per se did not influence survival. There was a significant increase in mortality in younger patients resulting from the severity of their underlying illness. We saw an increase in the number of complicating factors occurring at the onset of ARF that correlated with the increase in mortality. In survivors ARF was more prolonged in our most recent experience. The development of prolonged, complicated ARF and the poor survival seen in younger patients led to the increase in mortality in our patients.

Acute Kidney Injury↗
PubMed1985

Distribution studies of 111In-oxine-labeled peritoneal mononuclear cells in tumor-bearing rats.

We studied the distribution of 111In-labeled peritoneal mononuclear cells (PMC) in Sprague-Dawley rats with carcinosarcoma (CS) tumor. We obtained PMC from normal rats and rats pretreated with BCG or irradiated CS cells as antigenic stimulant. PMC were labeled in-vitro with 111In-oxine and transferred by tail-vein injection to rats bearing CS tumor. Twenty-four, 48 and 72 h after PMC transfer, we measured the accumulation of these cells in the CS tumor as a percentage of dose radioactivity per gram of tumor using an external gamma-ray camera. PMC from normal and BCG treated donor rats accumulated 0.4% and 0.46% dose per gram of CS tumor respectively. PMC from donor rats given killed CS cells accumulated significantly greater concentrations of 111In (0.79% dose per gram of CS tumor, P less than 0.025). Thus killed CS cells were able to sensitize the PMC of normal rats. 111In-oxine-labeling is an elegant procedure to study the distribution of mononuclear cells in tumors.

Animals↗
PubMed1985

A syndrome of chronic renal failure and XY gonadal dysgenesis in young phenotypic females without genital ambiguity.

A case of XY gonadal dysgenesis with renal failure is presented. Diagnosis was delayed four years post renal transplantation. A uterus, fallopian tubes, and vagina were present with a combined gonadoblastoma and dysgerminoma found in the right streak gonad. Six other similar cases have been reported, including concordance in a pair of monozygous twins. Because of the risk of gonadal malignancy, the serum FSH concentration should be determined in phenotypic females with primary amenorrhea and chronic renal disease. Due to a physiologic reduction in the serum FSH concentration in agonadal individuals between 5 and 11 years of age, a karyotype may be required to detect affected individuals during this interval. Gonadectomy should be performed in all cases of XY gonadal dysgenesis. A urinalysis and serum creatinine concentration should be obtained in girls presenting with XY gonadal dysgenesis. The serum FSH concentration and karyotype should be determined in females presenting with congenital nephrotic syndrome.

Adolescent↗
PubMed1985

Effects of low-protein diet on experimental diabetic nephropathy in the rat.

To evaluate the role of glomerular hyperfiltration in the development and progression of diabetic nephropathy, we performed clearance and histopathologic studies in 24 rats with streptozocin-induced diabetes after 3 months of diets with different protein compositions. Calcium phosphate was added to an 8% protein diet in group I (nine rats), and calcium carbonate to a 24% protein diet in group II (nine rats) to equalize calcium and phosphate contents in these diets. Group I and II rats also received small doses of insulin to reduce the excessive hyperglycemia induced by the high sucrose content of the diets. In group III, six rats given an 8% protein diet, no calcium, phosphate, or insulin was added. In groups I and III, low dietary protein significantly reduced glomerular filtration rate and renal plasma flow per gram of kidney weight as compared with rates observed in group II rats with a higher protein intake. Features of diabetic glomerulopathy including mesangial hypercellularity and mesangial matrix expansion were also significantly milder in the groups with a low protein diet. On the other hand, medullary calcification and interstitial changes were most prominent in group I, given calcium phosphate supplement; the increase in the kidney weight was greater in groups I and II, which received insulin, than in group III, which did not. It was concluded that low protein diet significantly ameliorates diabetic glomerulopathy but that supplementation with inorganic phosphate in an amount equal to organic phosphate contained in the higher protein diet causes medullary calcification and interstitial nephritis. Also, administration of suboptimal doses of insulin in diabetic animals greatly enhances renal growth, more than that induced by diabetes alone.

Animals↗
PubMed1983

Prospective trial of warfarin and dipyridamole in patients with membranoproliferative glomerulonephritis.

A prospective trial of warfarin and dipyridamole was performed in patients with membranoproliferative glomerulonephritis. Eighteen completed either a control or treatment year, and 13 completed both a control and treatment year. To obviate the bias of excluding control patients who had renal failure after one year, both an unpaired and a paired analysis were performed. The unpaired analysis compared 10 patients followed for an initial control year with eight patients receiving treatment first. Renal function remained stable over the year in the treated group, but worsened in the control group. Slopes of regression lines for reciprocal serum creatinine values were significantly different between groups (p less than 0.025). Urine protein excretion also decreased in the treated group. Four of 10 control patients had a two-fold increase in serum creatinine levels, but no treatment patient did. In the paired crossover analysis, significant differences in renal function were detected between control and treatment years in six patients whose renal function significantly changed over one of the years. In every instance, there was better preservation of renal function in the treatment year. Urinary protein also decreased significantly over the treatment year compared with the control year. Bleeding was the most frequent complication. These data suggest that warfarin and dipyridamole have a beneficial effect on renal function in membranoproliferative glomerulonephritis.

Adult↗
PubMed1983

Potentiation of nephrotoxic serum nephritis in Lewis rats by Freund's complete adjuvant--possible role for cellular immune mechanisms.

Lewis rats receiving subnephritic doses of nephrotoxic serum (NTS) showed increased albuminuria and glomerular histopathologic alterations during the autologous phase of nephrotoxic nephritis (NTN) when they received simultaneous footpad injections of Freund's complete adjuvant (FCA). Lymph nodal lymphocytes from such experimental rats showed increased in vitro cellular sensitization to the nephrotoxic IgG as measured by [3H]thymidine incorporation. Such a lymphocyte blastogenesis response was not detected in rats receiving the same doses of FCA or NTS alone. Antibody titers to the nephrotoxic rabbit IgG were not different in the two groups of rats as measured by enzyme-linked immunosorbent assay. The transfer of lymph nodal mononuclear cells from rats with NTN potentiated by FCA, was able to induce albuminuria and glomerular histopathologic alterations in recipients treated with NTS. In the above experimental model FCA appears to potentiate the autologous phase of NTN by cellular immune mechanisms.

Albuminuria↗
PubMed1983

Minimal change glomerular disease: a paraneoplastic syndrome in two patients with bronchogenic carcinoma.

Glomerulonephritis has often been reported as a paraneoplastic syndrome. In patients with carcinoma, the most common glomerular disease is membranous glomerulonephritis mediated presumably by immune complexes. Minimal change glomerular disease has been hitherto reported, to our knowledge, in only one patient with carcinoma. We report two patients with bronchogenic carcinoma in whom the simultaneous development of the nephrotic syndrome was due to minimal change glomerular disease.

Aged↗
PubMed1982

Type 3 membranoproliferative glomerulonephritis: clinicopathologic correlations and long-term follow-up in nine patients.

We studied the renal pathologic findings and results of long-term follow-up (four to 15 years; mean 7.8 years) in nine patients with type 3 membranoproliferative glomerulonephritis (MPGN). We selected these patients because biopsy specimens displayed extensive glomerular, subepithelial, electron-dense deposits, besides other changes characteristic of MPGN. We compared these patients with 14 others with type 1 MPGN similarly followed up for a period of 7.4 years. Patients with type 3 MPGN were older, had hypocomplementemia less often, and enjoyed a slightly better outcome. Although six patients with type 3 MPGN had the nephrotic syndrome, end-stage renal failure developed only in two, whereas it developed in five of the 14 patients with type 1 MPGN.

Adolescent↗
PubMed1981

Long-term therapy of uremic osteodystrophy in adults with calcitriol.

Patients with end-stage renal failure develop osteodystrophy in part due to defective production of 1,25-dihydroxycholecalciferol by the kidney. We treated eight adults with chronic renal failure and osteodystrophy with 1,25-dihydroxycholecalciferol (calcitriol) for 30-44 months. Seven of these patients were also symptomatic with bone pain and/or muscle weakness. Striking amelioration of muscle weakness occurred, and bone pain was considered to be significantly improved in four of seven patients. Hypercalcemia was noted in all the patients, necessitating a reduction in the daily dose of calcitriol to a range of 0.125 to 0.5 microgram/day. While serum alkaline phosphatase fell during therapy, serum iPTH did not show any significant change. Bone mineral content improved in four patients, though it still remained below normal. Radiographic changes of osteodystrophy showed definite improvement in only three.

Adult↗