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Biomedical subjects

M M Friedlaender

Publications and source records attributed to M M Friedlaender.

At least 19 recordsLinked to original sources
PubMed1992

Kidney transplantation in Jerusalem, 1972-89. Kidney Transplant Group.

The results of a small transplant program over 18 years are presented. Two hundred and fifty-six transplantations including 36 living donor transplants were performed in 203 patients. Graft survival at 1, 3, 5 and 10 years without and with cyclosporin A treatment was 57%, 49%, 44%, 38%, and 71%, 69%, 58%, -% (respectively). Patient survival was 83%, 67%, 62%, 54%, and 92%, 90%, 68%, -% (respectively). Recent results with cyclosporin A treatment have shown further improvement. Analysis using the COX model shows that age under 30 years, lack of systemic disease, and the use of cyclosporin A and living donors all improved patient survival. More than 10- and 5-year survival was achieved in 78 and 103 patients, respectively, of whom 53 and 81 have good graft function. Local transplant policy and patient material are discussed.

Adolescent↗
PubMed1989

The in vivo and in vitro effect of calmodulin antagonists on the renal actions of 25(OH) vitamin D3 in the rat.

Previous work from this laboratory has demonstrated that 25(OH) vitamin D3 [25(OH)D3] acutely suppresses the phosphaturic action of parathyroid hormone (PTH) and interferes with the PTH-induced activation of adenylate cyclase (AC). Calmodulin inhibitors block vitamin D-induced Ca2+ transport in the gut and phosphorus uptake in renal BBMV's. We have examined whether calmodulin antagonists affect the renal action of 25(OH)D3. Acute clearance experiments were performed in PTH-infused parathyroidectomized rats receiving 25(OH)D3 after pretreatment with trifluoperazine (TFP) or promethazine (P). In vitro PTH-induced activation of renal AC was also studied in membrane preparations from pretreated rats in the presence of 25(OH)D3. 25(OH)D3 reduced the PTH-stimulated increase in fractional excretion of phosphorus (CP/CIn) from 0.292 +/- 0.024 to 0.195 +/- 0.018 (p less than 0.005) and urinary cAMP from 149.3 +/- 20.3 to 78.1 +/- 10.4 pmol/min (p less than 0.01) and also blunted AC activation in vitro. TFP but not P abolished the effects of 25(OH)D3 both in vivo and in vitro. R 24571 also abolished the in vitro effect of 25(OH)D3. Thus, (1) TFP abolishes both the antiphosphaturic and the AC/cAMP-related actions of 25(OH)D3, (2) P does not have these effects, and (3) R 24571 abolishes the in vitro effect of 25(OH)D3. These results suggest that the antiphosphaturic effect of 25(OH)D3 acting via the AC/cAMP system may be calmodulin dependent.

Adenylyl Cyclases↗
PubMed1989

Oncogenous osteomalacia: a case study.

A case of oncogenous osteomalacia due to a fibrosarcoma of the maxilla is reported, with a 19 year course before treatment. Metabolic studies of calcium and phosphorus were performed 3 and 19 years after the first symptomology. There was a negative balance for both phosphorus and calcium with low serum levels of 1,25-dihydroxyvitamin D which were corrected by resection of the tumor. Portions of the tumor were cultured and the supernatant did not affect phosphorus transport by a proximal tubule kidney cell line. Other portions were injected into athymic nude mice where they resulted in hypophosphatemia and phosphaturia, thus confirming the endocrine nature of the oncogenous osteomalacia factor.

Adult↗
PubMed1989

Renal transplantation is not contraindicated in asymptomatic carriers of hepatitis B surface antigen.

Recent reports showing that the presence of positive tests for hepatitis B surface antigen (HBsAg) is associated with prohibitively high morbidity and mortality suggest that such patients should not be considered for kidney transplantation. The clinical outcome and serology including hepatitis B DNA assays of 11 patients who were HBsAg-positive at the time of transplantation, as well as the hepatic complications in all 200 kidney transplantations during the same period, were analyzed. In the 11 HBsAg-positive patients, no clinical or laboratory evidence suggesting deterioration in liver function over a mean follow-up period of 8.0 +/- 1.7 years was found. Of six patients with fatal or severe chronic liver disease, only one was HBsAg-positive at the time of transplantation and showed no deterioration over 9 years. Two immunosuppressed patients developed anti-HBs antibodies after acute hepatitis B infection. A review of the literature leads to the conclusion that previous reports of poor patient prognosis may represent patients who first showed HBsAg positivity after transplantation or who had preexisting HBsAg-related liver disease. The present findings suggest that asymptomatic patients with positive tests for HBsAg should not be excluded from kidney transplantation programs.

Adult↗
PubMed1989

Calcium regulates parathyroid hormone messenger ribonucleic acid (mRNA), but not calcitonin mRNA in vivo in the rat. Dominant role of 1,25-dihydroxyvitamin D.

In vivo 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) decreased PTH and calcitonin gene transcription. A low calcium is the major signal for PTH secretion, and a high calcium for calcitonin secretion. We report here that calcium has no effect on calcitonin messenger RNA (mRNA) levels in vivo in the rat, but that a low calcium markedly stimulates PTH mRNA levels. Serum calcium was decreased by ip phosphorus and increased by calcium gluconate (ip or iv infusion) and demonstrated that a low serum calcium markedly increased PTH mRNA levels whereas a high serum calcium had no effect. There was no change in mRNAs for calcitonin or actin in the same thyroparathyroid extracts. After phosphorus ip serum calcium decreased from 10.4 to 8.5 mg/dl and PTH mRNA increased up to 3-fold at 1, 3, and 6 h. Gel blots showed that a low calcium increased PTH mRNA levels with no change in its size (833 base pairs). Calcitonin ip decreased both serum calcium and phosphorus with an up to 5-fold increase in PTH mRNA at 1 h, thus demonstrating that the effect of phosphorus on PTH mRNA was due to the low serum calcium and not the high serum phosphorus. When phosphorus and 1,25(OH)2D3 (100 pmol/100 g) were injected together, despite the low serum calcium, there was a decrease in PTH mRNA levels. These results show a linear relationship between calcium and PTH gene expression, but not calcitonin or actin, with a dominant role for 1,25(OH)2D3.

Animals↗
PubMed1988

Noninvasive assessment of skin iron content in hemodialysis patients. An index of parenchymal tissue iron content?

Iron overload has been described in patients undergoing chronic hemodialysis. The present study was undertaken to evaluate a rapid, noninvasive method for determination of skin iron by the technique of diagnostic x-ray spectrometry (DXS). Thirty-five patients receiving chronic hemodialysis treatment entered the study and were compared with 25 normal controls. Since pathological skin iron deposition occurs mainly at the dermal-epidermal junction in the basal cells of the epidermis, measurements were made in the thenar eminence representing mainly epidermal tissue (FeE), and in the forearm representative mainly of dermis (FeD). The mean +/- SD FeE iron concentrations were equivalent to 14.5 +/- 8.8 and 18.2 +/- 10.2 parts per million wet weight tissue (ppm) and both were significantly higher than in normal controls in which they averaged 9.2 +/- 2.5 ppm (P less than 0.005) and 10.2 +/- 3.2 ppm (P less than 0.001), respectively. There was significant positive correlation between individual skin iron determinations with the total number of blood transfusions received, the rate of blood transfusion, and with serum ferritin levels. Bone marrow hemosiderin was examined in six patients and showed a similar trend. Despite correlation only with indirect indices of tissue iron, our findings suggest that DXS may serve as a reliable quick method for noninvasive estimation of nonreticuloendothelial tissue iron deposition in hemodialysis patients suspected of having transfusional iron overload. The method may be valuable in monitoring the effects of chelation therapy.

Adult↗
PubMed1988

Colchicine does not interfere with the antiphosphaturic effect of 25(OH) vitamin D3 in the rat.

The effect of colchicine pretreatment on the antiphosphaturic action of 25(OH)vitamin D3 (25[OH]D3) was examined in parathyroidectomized (PTX), parathyroid-hormone (PTH)-infused rats by acute clearance studies. The following groups were studied: group 1, colchicine-pretreated PTX rats; group 2, colchicine-pretreated PTX rats receiving PTH infusion; group 3, colchicine-pretreated PTH-infused PTX rats receiving intravenous 25(OH)D3 with pretreated PTH-infused PTX rats serving as controls. The effect of 25(OH)D3 on PTH-activated renal adenylate cyclase [AC] from colchicine-pretreated rats was studied in vitro. In group 1, fractional excretion of phosphate (Cp/CIn) after colchicine was 0.102 +/- 0.011 vs. 0.029 +/- 0.005 in controls (p less than 0.001). In group 2, PTH increased Cp/CIn from 0.074 +/- 0.026 to 0.184 +/- 0.028 (p less than 0.05) in colchicine-pretreated animals and from 0.018 +/- 0.006 to 0.213 +/- 0.034 in controls (p less than 0.0025). In group 3, 25(OH)D3 decreased Cp/CIn from 0.344 +/- 0.022 to 0.235 +/- 0.026 (p less than 0.005) and UcAMP from 103.7 +/- 12.4 to 69.0 +/- 9.6 (p less than 0.025). In vitro PTH activation of AC was blunted in colchicine-pretreated rats; however, the response to 25(OH)D3 was intact. Histological changes compatible with microtubule disruption were found in proximal tubules of kidneys from colchicine-pretreated rats. These results show that colchicine alters the response to PTH but it does not affect the antiphosphaturic action of 25(OH)D3, suggesting that this action is not mediated via cytoplasmic microtubules.

Adenylyl Cyclases↗
PubMed1988

Impaired production and decreased urinary excretion of adenosine 3',5'-monophosphate in primary hyperparathyroidism with vitamin D deficiency.

Increased urinary excretion of cAMP is a common finding in patients with primary hyperparathyroidism. We report a patient with hypercalcemia, primary hyperparathyroidism, vitamin D deficiency and high nephrogenous cAMP that fell to low levels during the course of a protracted illness. Surgical removal of a large parathyroid cystic adenoma was associated with a decrease in plasma calcium. Because of the relatively low nephrogenous cAMP with high plasma iPTH the biological activity of the fluid aspirated from the adenoma was examined. Acute clearance studies were performed in parathyroidectomized rats and their response to the parathyroid fluid was compared with the response of synthetic PTH. Similar phosphaturic responses to PTH and the aspirated fluid were recorded and were preceded by similar increments in nephrogenous cAMP. Thus the discrepancy between the high plasma calcium, high PTH and the low nephrogenous cAMP seen in our patient was related to impaired cAMP production by the renal adenylate cyclase. There was no evidence for a hormone with a different biological activity. The impaired formation of cAMP may reflect a combined result of several factors including downregulation of renal adenylate cyclase, phosphate depletion and vitamin D deficiency state.

Adenoma↗
PubMed1988

Effect of intravenous glucagon on the urinary excretion of adenosine 3',5'-monophosphate in man and in rats. Evidence for activation of renal adenylate cyclase and formation of nephrogenous cAMP.

To examine the effect of glucagon in vivo on renal formation and excretion of cAMP, clearance studies were performed in patients with hypoparathyroidism and in parathyroidectomized rats. Four patients with idiopathic hypoparathyroidism and 2 patients with pseudohypoparathyroidism were studied during an intravenous glucagon infusion (20 micrograms/kg body weight). In all patients, glucagon induced a significant increase in nephrogenous cAMP and a 2- to 3-fold increase in fractional excretion of phosphate. The average increase in nephrogenous cAMP was from a baseline of 784 +/- 229 to 18,748 +/- 3,842 pmol/100 ml glomerular filtrate (GF) (p less than 0.01) and occurred 30-60 min after the beginning of the glucagon infusion. The effect of intravenous glucagon, given as a bolus, was further examined in parathyroidectomized rats. Glucagon elicited a significant increase in the urinary excretion of the nucleotide. The excreted cAMP was compared with its filtered load for each urine collection period. In the first two collections, 0-15 and 15-30 min, the filtered load of cAMP was higher than its urinary excretion. During the following periods, 30-90 min, the excreted urinary cAMP exceeded by far its filtered load, suggesting a net nephrogenous contribution to the excretion of the nucleotide. Infusion of exogenous cAMP to parathyroidectomized rats induced significant increments in the filtered load and urinary excretion of the nucleotide. Tubular secretion of extrarenal cAMP could not be detected during the cAMP infusion. These results provide evidence supporting in vivo a possible parathyroid-independent formation of nephrogenous cAMP after glucagon administration, in men and in rats. The glucagon-induced increase in nephrogenous cAMP seems to account, at least partly, for some of the renal actions of this hormone.

Adenylyl Cyclases↗
PubMed1987

Renal biopsy in Fabry's disease eight years after successful renal transplantation.

Late graft histology after renal transplantation for Fabry's disease has only once been previously reported. Clinical data and kidney biopsy findings in a case of Fabry's disease before and eight years after successful kidney transplantation are presented. The graft maintains normal function. Graft histology in light microscopy showed no abnormalities reminiscent of the diseased native kidney. Electron microscopy revealed occasional small myelin figures which were present only in the vascular endothelium. Their significance and a review of conflicting reports and opinions from the literature are discussed.

Adult↗
PubMed1986

Progressive vascular calcification with necrosis of extremities in hemodialysis patients: a possible role of iron overload.

Progressive vascular calcification with ischemia and gangrene of the extremities occurs rarely in uremic patients, patients undergoing maintenance dialysis, and following renal transplantation. In this paper we present two additional patients on chronic hemodialysis who developed this syndrome in association with severe secondary hyperparathyroidism. Fulminant gangrene led to the death of the first patient, while in the second, multiple amputations had to be performed after parathyroidectomy. In both patients, evidence of iron overload due to multiple blood transfusions was present and iron was histologically demonstrated in a calcification area in one case. The possibility of iron overload as a "challenger" for systemic calciphylaxis is discussed.

Acute Disease↗
PubMed1986

Combined cyclophosphamide and corticosteroid-induced remission in severe glomerulopathy associated with systemic vasculitis.

Three patients with systemic vasculitis and severe renal disease as major manifestations are reported. In 2 cases, rapidly progressive glomerulonephritis presented as oliguric renal failure. In the third case, the clinical picture was severe nephrotic syndrome with decreased renal function. Combined cyclophosphamide and corticosteroid treatment resulted in dramatic improvement of renal function and remission of nephrotic syndrome. In 2 cases, histological improvement was documented by repeated kidney biopsy. The optimal duration of cyclophosphamide therapy has to be determined.

Adult↗
PubMed1986

IgA nephropathy and acute reversible renal failure.

Macroscopic hematuria, severe oliguria for 9 days, and azotemia requiring a period of hemodialysis treatment developed in a young woman. Renal biopsy during the acute episode showed IgA nephropathy with blockage of tubules by red cell casts and tubular epithelial cell damage. Renal function recovered spontaneously. The severity of the renal failure was unique, and this syndrome should be added to the other known causes of acute reversible renal failure.

Acute Kidney Injury↗
PubMed1985

The effect of acute saline volume expansion on renal Na-K-ATPase.

To examine the role of Na-K-ATPase in the natriuresis that occurs after acute extracellular volume expansion, we performed acute clearance experiments and in vitro analysis of renal microsomal ATPase activity in rats receiving intravenous 0.9% sodium chloride (0.1 ml/100 g bw/min). Despite increased absolute reabsorption of filtered sodium (196 +/- 8.1 vs. 165 +/- 11.4 uEq/min, p less than 0.05), renal medullary microsomal Na-K-ATPase activity was decreased from 134 +/- 5.9 to 110 +/- 6.3 pmol Pi/mg protein/hour (p less than 0.02). No changes occurred in cortical or papillary regions and Mg-ATPase was unaffected. Similar results were obtained after adding 4 mEq/l potassium chloride to the infusion to prevent any fall in serum K+. These data suggest that a considerable percentage of sodium reabsorption is suppressed in acutely volume expanded animals and it is proposed that this is mediated by inhibition of medullary Na-K-ATPase.

Animals↗