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Biomedical subjects

D Rubinger

Publications and source records attributed to D Rubinger.

At least 37 records · Page 2Linked to original sources
PubMed1987

IgM nephropathy: morphological study related to clinical findings.

This study describes 10 cases of IgM nephropathy in whom the main morphological findings consisted of diffuse mesangial deposition of IgM and varying degrees of mesangial cell proliferation. In addition, focal segmental sclerosis was present in 1 patient and global sclerosis in another. An ill-defined electron-dense deposit was seen within the mesangial area in 1 case. Except for 1 patient, who had hematuria only, all suffered from nephrotic syndrome without deterioration of renal function. In view of the constant and characteristic finding of a diffuse mesangial IgM deposition, it is suggested that this form of nephropathy constitutes an entity separate from focal glomerulosclerosis or minimal change disease.

Adolescent↗
PubMed1987

24,25(OH)2D3 attenuates the calcemic effect of 1,25(OH)2D3 in rats with reduced renal mass.

The present study was undertaken to evaluate the effect of 24,25(OH)2D3 on serum calcium concentration in rats with reduced renal mass. Adult 5/6 nephrectomized male rats were divided into four groups: (i) control rats, (ii) rats treated with 1,25(OH)2D3, (iii) rats treated with 24,25(OH)2D3, and (iv) rats treated with 1,25(OH)2D3 and 24,25(OH)2D3. After 4 days, serum calcium in the 1,25(OH)2D3-treated group was 7.13 +/- 0.32 meq/liter (P less than 0.001 vs control). With the combination of 1,25(OH)2D3 and 24,25(OH)2D3 serum calcium was higher than that in control, 6.25 +/- 0.5 meq/liter (P less than 0.001 vs control), but lower than that in rats receiving 1,25(OH)2D3 alone (P less than 0.05). No change in serum calcium was seen in animals treated with 24,25(OH)2D3 alone. On the eighth day serum calcium in the 1,25(OH)2D3-treated group, 6.52 +/- 0.25, was higher than in the 1,25(OH)2D3 + 24,25(OH)2D3 group, 5.87 +/- 0.17 meq/liter, P less than 0.05, P less than 0.001 vs control. In both 1,25(OH)2D3- and 1,25(OH)2D3 + 24,25(OH)2D3-treated rats, hypercalciuria of similar magnitude occurred on the fourth and eighth day of treatment. No change in urinary calcium was seen in the control and 24,25(OH)2D3-treated rats. Thus, in 5/6 nephrectomized rats combined administration of 1,25(OH)2D3 and 24,25(OH)2D3 attenuates the calcemic response to 1,25(OH)2D3 without changes in urinary calcium excretion. These observations suggest that the effect of 24,25(OH)2D3 on serum calcium is different in 5/6 nephrectomized rats as compared to normal rats, in which an augmentation of serum calcium was observed following administration of both vitamin D metabolites. The effect of 24,25(OH)2D3 on serum calcium in rats with reduced renal mass may result from a direct effect of 24,25(OH)2D3 on the bone.

24,25-Dihydroxyvitamin D 3↗
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↗
PubMed1987

Renal handling of phosphate during extracellular volume expansion and parathyroid hormone administration.

To further examine the interaction between the phosphaturic effects of parathyroid hormone (PTH) and extracellular volume expansion (ECVE), clearance studies were performed in chronically and acutely parathyroidectomized (PTX) rats in three sets of experiments. In the first series, two groups of chronically PTX animals (groups 1 and 2) received a PTH infusion (2 U/h). In group 1 ECVE was superimposed on the PTH infusion, while the animals in group 2 received the hormone infusion alone. In the second series the following groups of chronically PTX rats were examined: volume expanded rats (groups 3 and 4) and control normovolemic rats (group 5). A PTH bolus (5 units) was added to group 3 while group 4 underwent volume expansion alone. The third series of experiments compared the response of acutely and chronically PTX rats given a submaximal dose of PTH (1 U/h) with additional ECVE (group 6) or undergoing submaximal ECVE with additional PTH (group 7). In the first set of experiments, the PTH-ECVE rats had a higher inulin clearance (CIn) and phosphate clearance (Cp) than the animals receiving the PTH alone. The maximal fractional excretion of phosphate (Cp/CIn) was similar in both groups. In the second set, GFR was similar in the normovolemic and the volume expanded animals. The two volume expanded groups had a higher Cp/CIn than the control normovolemic animals. The maximal Cp/CIn was 0.234 +/- 0.031 in the ECVE-PTH and 0.235 +/- 0.056 in the ECVE animals (p = NS). No significant difference could be detected during the whole experiment in any variable between the volume-expanded PTH-injected (ECVE-PTH) and ECVE only rats. Acutely and chronically PTX rats responded with a similar degree of phosphaturia after ECVE superimposed on PTH infusion or after PTH superimposed on ECVE. Acutely PTX rats, however, exhibited a significantly delayed response to exogenous PTH as compared to chronically PTX animals. There was no difference in the response to ECVE between the acute and chronically PTX rats. When chronically PTX rats were exposed to submaximal ECVE, the final Cp/CIn was less than after ECVE-PTH, PTH-ECVE or PTH. These findings show that in chronically PTX rats the phosphaturic response to PTX and ECVE is not additive under conditions of maximal stimulation by PTH or ECVE. Examination of acutely PTX animals and use of a different protocol of ECVE disclose a broader spectrum of phosphaturic responses.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
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 suppression of prostaglandin synthesis on renal function in rats with intact and reduced renal mass.

The present study was undertaken to assess the role of prostaglandin system in the compensatory response to reduced nephron population, respective to renal function and electrolyte excretion. Intact and 5/6 nephrectomized rats were divided in 4 groups: 1) rats pretreated with indomethacin, 2) rats pretreated with the vehicle of indomethacin, 3) rats pretreated with sulindac, and 4) rats pretreated with the vehicle of sulindac. In normal rats, indomethacin administration resulted in a mild decrease in creatinine clearance and a significant reduction of the urinary Na excretion. In the rats with reduced renal mass treated with indomethacin, the creatinine clearance did not differ from that in the control group. The 24 h urinary sodium excretion and the fractional excretion of sodium, however, were significantly lower in the indomethacin treated animals than in the control rats. No change in the creatinine clearance or in the sodium excretion was observed in all groups pretreated with sulindac. The urinary PGE2 and thromboxane excretion was significantly lower in the indomethacin treated intact rats and the rats with reduced renal mass. Sulindac induced a slight decrease in urinary excretion of PGE2 in intact rats. No significant change in urinary excretion of PGE2 or thromboxane was seen after sulindac in the rats with reduced renal mass. The antinatriuretic effect of indomethacin was dissociated from changes in urine flow in all groups of animals, suggesting that the increase in Na reabsorption took place in a water impermeable segment of nephron. These results suggest that the compensatory increase in urinary Na excretion per nephron in rats with reduced nephron population at least partly depends on an intact prostaglandin synthesis.

Animals↗
PubMed1985

Vitamin D-dependent rickets types I and II. Diagnosis and response to therapy.

The diagnostic value of measuring serum vitamin D metabolites is demonstrated in the present study in which two patients with vitamin D-dependent rickets (VDDR) Types I and II are reported. The patient with sporadic VDDR Type I was severely disabled and unable to walk. Her serum 1,25(OH)2D level was low (32 pg/ml, normal 30 to 60) and she responded dramatically to 1 microgram of 1 alpha-hydroxyvitamin D3 daily. The VDDR Type II patient had an autosomal recessive inheritance and total alopecia. His serum 1,25(OH)2D level was greater than 500 pg/ml, compatible with end-organ refractoriness to 1,25(OH)2D. He did not respond to daily doses of 1 microgram 1 alpha-hydroxyvitamin D3. These cases demonstrate the striking difference in 1,25(OH)2D levels and therapeutic response to 1,25(OH)2D in these two conditions.

Adult↗
PubMed1983

Sodium-dependent idiopathic hypercalciuria in renal-stone formers.

Four patients with renal stones had hypercalciuria which was dependent on a high sodium intake. Moderate sodium restriction corrected the hypercalciuria. Sodium excretion should be measured in all patients with idiopathic hypercalciuria so that the easily treated sodium-dependent hypercalciuria can be diagnosed.

Adult↗
PubMed1983

Frontal lobe calcification in hypoparathyroid states.

Basal ganglion calcification is common in hypoparathyroid states. However, cerebral cortical calcification is rarely seen. Of the six cases previously recorded, five were in patients with idiopathic hypoparathyroidism and only one in a patient with pseudohypoparathyroidism. The present report is of a second case of pseudohypoparathyroidism with cerebral cortical calcification. It is stressed that cortical calcification occurs predominantly in the frontal lobes.

Adult↗
PubMed1976

Quinidine hypersensitivity and liver involvement. A survey of 32 patients.

Thirty-two of 487 patients who received quinidine between the years of 1970 and 1974 in the departments of medicine at Hadassah University Hospital developed hypersensitivity reactions. Ten of the 32 patients had clinical and biochemical manifestations of liver invlovement. In 4 patients liver biopsy showed granulomatous hepatitis. It is therefore concluded that quinidine-induced hepatitis is a relatively common side effect of this drug.

Chemical and Drug Induced Liver Injury↗