PubMed Health⌕ Search

Biomedical subjects

J B Puschett

Publications and source records attributed to J B Puschett.

At least 91 records · Page 5Linked to original sources
PubMed1980

Dissociative effects of piretanide on proximal tubular PO4 and HCO3 transport.

The effect of piretanide on renal electrolyte transport was evaluated by simultaneous micropuncture and clearance studies. In chronically thyroparathyroidectomized (TPTX) dogs, the drug caused an increased percentage excretion (%E) of sodium (from 0.6 +/- 0.1 to 15.2 +/= 1.8%, P less than 0.01) as well as of calcium (from 1.0 +/- 0.2 to 17.8 +/- 1.7%, P less than 0.001) and bicarbonate (from 1.2 +/- 0.4 to 5.9 +/- 0.9, P less than 0.001), but there was no change in %E of phosphate (4.0 +/- 0.9 to 6.6 +/- 1.6, P less than 0.10). In the presence of a constant infusion of parathyroid hormone (PTH) the drug caused a greater degree of natriuresis, calciuria, and bicarbonaturia and a significant increase in %E of PO4 (from 7.4 +/- 1.6 to 20.0 +/- 2.1, P less than 0.05). Proximal fractional reabsorption (PFR) of PO4 was unaffected, but there was a significant decrease in PFR of sodium, calcium, and bicarbonate in the TPTX dogs. The presence of PTH did not alter the effects of piretanide on PFR of phosphate and bicarbonate. There was no change in urinary or tubular fluid pH in either group of dogs. These data indicate that piretanide dissociates proximal PO4 transport from that of sodium and bicarbonate. In the presence of PTH, the drug inhibits PO4 transport beyond the late proximal convoluted tubule. In addition, tubular (and urinary) pH appears to be an important regulator of PO4 transport, especially in the absence of PTH.

Animals↗
PubMed1980

Therapy of renal osteodystrophy with dihydrotachysterol in non-dialyzed patients.

Two non-dialyzed patients with severe uremic bone disease were treated successfully with dihydrotachysterol (DHT). In each case, dramatic clinical improvement was noted in several weeks and this was verified by biochemical, radiologic and histologic measurements. Although DHT has been utilized previously in combination with dialysis, its documented effectiveness in the absence of the latter therapy has not previously been reported.

Adult↗
PubMed1980

Peritonitis in chronic peritoneal dialysis patients.

The incidence, etiology and management of peritoneal infection were evaluated in a chronic peritoneal dialysis population at a private community referral hospital. An initial incidence of peritonitis of 10.8% in early 1976 was reduced to a rate of 0.19% in the latter half of 1978. Factors associated with this decline were: establishment of a separate peritoneal dialysis unit; strict adherence to aseptic technique; and the replacement of manual procedures with automated equipment. Preliminary results suggested also that antibiotic therapy of asymptomatic patients with culture-positive dialysis return may be an additional effective method for the prevention and control of peritonitis in this patient population.

Anti-Bacterial Agents↗
PubMed1979

Acute effects of piretanide in normal subjects.

Acute clearance studies were performed in normal subjects to assess the actions of the new diuretic, piretanide, on renal function. The drug increased both glomerular filtration rate and effective renal plasma flow in roughly proportionate amounts, so that filtration fraction did not change. In a dosage of 2 to 3 mg, it induced an increase in sodium excretion of almost 13% of filtered load, and there was an associated 2- to 3-fold increase in potassium excretion. The abstraction of solute-free water from the collecting duct was markedly reduced, but the drug induced no significant decline in the generation of free water. The rate of bicarbonate excretion, as well as that of titratable acid and ammonium, was increased approximately proportionately so that there was no increase in urinary pH or net hydrogen ion excretion. There was no phosphaturia, a unique finding, since all other drugs and maneuvers that cause a bicarbonate diuresis are also phosphaturic. Piretanide increased calcium excretion by approximately 19% of filtered load. The data suggest that the drug acts largely in the ascending limb of the loop of Henle and that it also affects the proximal tubule. Despite its sulfonamide structure, none of the drug's effects appear to be related to inhibition of carbonic anhydrase.

Diuretics↗
PubMed1979

Diabetic nephropathy as the mode of presentation of diabetes mellitus.

Diabetic nephropathy have only rarely been described in patients who have minimal or no glucose intolerance. We herein report the case of a 59-yr-old man who presented with nephrotic syndrome and minimal glucose intolerance whose renal biopsy showed the nodular (Kimmelsteil-Wilson) and diffuse glomerulosclerosis lesions characteristic of diabetes. We critically review the literature on this subject, pointing out the pitfalls in diagnosis and establishing strict criteria for the diagnosis of diabetic nephropathy in patients wihout overt clinical diabetes.

Basement Membrane↗
PubMed1979

Differential effects of diuretic agents on electrolyte excretion in the dog. Role of renal hemodynamics.

The sulfonamide derivative diuretics acetazolamide, metolazone and furosemide produce differing degrees of natriuresis and varying patterns of phosphate excretion. At least part of the explanation for these diverse actions could be related to divergent effects of the drugs on total renal blood flow (TRBF) and its intracortical distribution (IBFD). To test this hypothesis, and to determine if a consistent thesis regarding alterations in interenal blood flow could be developed, clearance studies were performed in chronically thyroparathyroidectomized dogs in which radioactive microsphere methodology was utilized to evaluate the distribution of blood flow within the renal cortex. These data were then compared with those available in the literature. The variations which the drugs induced in TRBF and IBFD did not help to explain the differences in their diuretic actions. However, a consistent hypothesis relating natriuresis, perfusion pressure, renal vascular resistance, TRBF and IBFD could be developed based on the data from this study and those available in the literature.

Acetazolamide↗
PubMed1978

Vitamin D metabolism and expression in rats fed on low-calcium and low-phosphorus diets.

1. Cholecalciferol, radioactively labelled with both (14)C and (3)H, was administered weekly for 7 weeks to rats that had been depleted of vitamin D for 4 weeks before repletion with the radioactive vitamin. This permitted measurement of the steady-state effect on vitamin D metabolism of low-calcium and low-phosphorus regimens, as compared with a normal mineral intake. These dietary manoeuvres were carried out during the last 3 weeks of repletion. Cholecalciferol, 25-hydroxycholecalciferol and 1,25-dihydroxycholecalciferol were determined in plasma, intestine, kidney and bone. Ca(2+)-binding-protein content was measured in intestine and kidneys of comparable animals. 2. In rats on the low-calcium diets, 1,25-dihydroxycholecalciferol concentration was elevated in plasma, bone, kidney and intestine, and intestinal Ca(2+)-binding protein was increased to over twice the concentration found in the control animals. 3. The low-phosphorus regimens led to a decrease in plasma phosphate and 1,25-dihydroxycholecalciferol in all tissues studied, for the latter to the point where it was undetectable in plasma and bone. Intestinal and renal concentrations of Ca(2+)-binding protein were unchanged in the low-phosphate-intake group and decreased in the very-low-phosphate-intake group. 4. It is concluded that in the rat, unlike in the chick, hypophosphataemia is not associated with a stimulation of the production of 1,25-dihydroxycholecalciferol or its expression in the synthesis of Ca(2+)-binding protein. Therefore the plasma phosphate concentration does not appear to be directly involved in the regulation of the functional metabolism of vitamin D.

Animals↗
PubMed1978

Uncoupling of proximal sodium bicarbonate from sodium phosphate transport by bumetanide.

Re-collection micropuncture of late proximal tubular segments and simultaneous clearance studies were performed in chronically thyroparathyroidectomized dogs before and after the intravenous administration of bumetanide. The drug, a new sulfonamide-derivative diuretic, inhibited proximal fractional sodium and fluid transport by 0.12 (from 0.44 +/- 0.04 to 0.32 +/- 0.04, P less than 0.05) and that of bicarbonate by 0.14 (from 0.43 +/- 0.05 to 0.29 +/- 0.07, P less than 0.02). Tubular fluid bicarbonate concentration was unchanged, indicating a reduction in the transport of this ion proportionate to that of tubular fluid. However, unlike sodium and bicarbonate reabsorption, fractional proximal phosphate transport was unaltered (from 0.65 +/- 0.04 to 0.62 +/- 0.04, P greater than 0.40). The drug induced a substantial natriuresis; the percentage of filtered sodium excreted rose from 0.4 +/- 0.1 to 13.1 +/- 2.4% (P less than 0.005). Bicarbonate and phosphate excretion rose more modestly: the percentage excretion of the former ion increased from 0.9 +/- 0.3 to 3.7 +/- 0.08% (P less than 0.005) and that for phosphate doubled (from 3.4 +/- 1.0 to 6.8 +/- 1.3%, P less than 0.025). However, urinary pH did not change. Accordingly, bumetanide uncoupled the transport of sodium bicarbonate from that of sodium phosphate in the proximal convoluted tubule. It is concluded from these data that the action of bumetanide in the proximal convoluted tubule is probably not related either to carbonic anhydrase inhibition or to the impairment of sodium-phosphate-linked transport.

Animals↗
PubMed1977

Relationship between serum phosphate concentration and proximal tubular bicarbonate transport.

Micropuncture studies were performed in intact and thyroparathyroidectomized (TPTX) dogs to evaluate the relationship between the absolute level of serum ultrafilterable phosphate concentration (SUFP) and proximal bicarbonate reabsorption. In both groups of animals, a reverse linear relationship was noted between the serum phosphate level and the tubular fluid bicarbonate concentration (TFHCO3). For the intact dogs, TFHCO3=32.27 SUFP+/-2.17, r=0.715, p=0.02, and for the TPTX dogs, TFHCO3=35.68-2.39 SUFP+/-2.26; r=0.619, p less than 0.02. Furthermore, when late-proximal tubular values for absolute bicarbonate reabsorptive rate (THCO3)/100 nl single nephron filtrate were plotted against SUFP, a direct relationship was found for both groups; intact dogs: THCO3=205 SUFP-169+/-136, r=0.707, p less than 0.05; TPTX dogs: THCO3=224 SUFP-882+/-221, r=0.625, p less than 0.01. Variations in plasma bicarbonate concentration or PCO2 did not contribute to the relationship between SUFP and bicarbonate reabsorption. The data suggest that extracellular fluid phosphate concentration is an important modulator of proximal bicarbonate transport, independent of the action of parathyroid hormone.

Animals↗
PubMed1977

Study of the sites and mechanisms of action of bumetanide in man.

Acute clearance studies were performed in normal subjects to establish the site(s) and mechanism of action of the new diuretic agent, bumetanide (3-n-butylamino-4-phenoxy-5-sulfamylbenzoic acid), in the human kidney. When the drug was administered during water diuresis, solute-free water formation was unchanged associated with a peak increment in fractional sodium excretion of approximately 15% of filtered load. However, studies performed in hydropenic subjects demonstrated a virtual abolition of free water reabsorption. The diuretic caused a mild phosphaturia which did not appear to be related to alterations in parathyroid hormone. Furthermore, whereas net hydrogen ion excretion and urinary pH were unchanged, the excretion of ammonium ion, titratable acidity and bicarbonate all increased mildly. Taken together, the data suggest that the primary site of action of bumetanide is the medullary portion of the ascending limb of the loop of Henle, but that in addition, bumetanide inhibits the transport of sodium in the proximal nephron. Despite the fact that the drug is a sulfonamide derivative, its proximal activity seems unrelated to a carbonic anhydrase inhibitory effect. More likely the agent interferes with proximal reabsorption by impairing sodium-phosphate linked transport.

Administration, Oral↗