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R D Zipser

Publications and source records attributed to R D Zipser.

66 records · Page 4Linked to original sources
PubMed1978

Release of immunoassayable prostaglandin E by the human ischemic kidney.

Immunoassayable prostaglandin E concentration in renal venous plasma was measured in eight patients with renovascular hypertension. Two subjects with bilateral renal artery stenosis had similar concentrations from both renal veins. The six subjects with unilateral artery stenosis had greater concentration on the stenotic side in each case, suggesting that the human ischemic kidney produces increased amounts of prostaglandins.

Humans↗
PubMed1978

The prostaglandin and kallikrein-kinin systems in mineralocorticoid escape.

To evaluate the interactions of the renal prostaglandin and kallikrein-kinin systems during mineralocorticoid escape, we administered desoxycorticosterone acetate (DOCA; 20 mg im daily for 10 days) to five normal men and then repeated the study 2-16 weeks later with simultaneous indomethacin (200 mg/day) or ibuprofen (1600 mg/day) for prostaglandin inhibition (PI). Plasma aldosterone, PRA, and urinary prostaglandin E (PGE) were measured by immunoassay; urinary kallikrein activity was measured by esterase activity. With DOCA, subjects gained 2.0 +/- 0.1 (SE) kg and retained 485 +/- 125 milliequivalents (meg) sodium; serum potassium fell from 4.6 +/- 0.2 to 3.2 +/- 0.1 meq/liter, aldosterone fell from 3.8 to 2.2 ng/dl, and PRA fell from 0.9 to 0.1 ng/ml . h (all P less than 0.05). Kallikrein increased from 6.4 +/- 1.6 to 65.3 +/- 18.8 esterase U (P less than 0.01), but PGE (820 +/- 110 vs. 780 +/- 80 ng/day) did not change. With DOCA and PI, PGE fell by 80%. Subjects again gained 2.0 kg and retained 530 +/- 106 meq sodium; aldosterone fell to 1.1, PRA fell to 0.2, and potassium fell to 3.3 (all P less than 0.05 from basal, but P less than 0.4 from DOCA alone). Kallikrein again rose to 56.0 +/- 19.2 (P less than 0.01). However, the rate of sodium retention was enhanced slightly but significantly. These studies demonstrate that with DOCA, urinary kallikrein activity increases but PGE is unaltered. The minimal effects of prostaglandin inhibition and the lack of change in PGE excretion suggest that prostaglandins do not play an important role in mineralocorticoid escape. There is no apparent interaction of prostaglandins with the kallikrein system in this model; however, the kallikrein-kinin system may still play a direct role in the escape phenomena.

Adult↗
PubMed1976

Tuberculous pseudotumors of the liver.

A 35 year old man presented with fever, weight loss and adenopathy. The clinical presentation, laboratory studies, liver scan and laparotomy all suggested metastatic carcinoma. Bacteriologic and pathologic studies established a diagnosis of macronodular tuberculosis isolated to the liver. Response to antituberculous drug therapy was rapid. Review of the literature revealed this case to be a rare example of tuberculous pseudotumors of the liver.

Adult↗
PubMed1976

The effect of ACTH and cortisol on aldosterone and cortisol clearance and distribution in plasma and whole blood.

The mechanisms of increased aldosterone and cortisol metabolic clearance rates (MCR) following ACTH or cortisol administration were studied in 13 subjects undergoing cardiac catheterization and in 9 healthy controls. In control subjects, the MCR (plasma) of both steroids increased by 29% (aldosterone: from 936 +/- 57 to 1204 +/- 55 l/day/m2, cortisol: from 205 +/- 12 to 264 +/- 17 l/day/m2 +/- SE) after ACTH (12 units/h) for 1 to 4 h, and by 20 and 32%, respectively, after cortisol (12 mg/h) for 1 to 2 h. In contrast, aldosterone MCR (whole blood) did not change with ACTH or cortisol administration (from 1276 +/- 57 to 1330 +/- 59 l/day/m2), indicating that the plasma MCR increase results from a redistribution of aldosterone from plasma to red cells. Aldosterone splanchnic extraction was 92 +/- 1% (n = 12) with normal morning cortisol levels, and extraction was unchanged after ACTH administration. For cortisol, however, the splanchnic extraction increased from 8 +/- 0.8% to 17.8 +/- 5.0%, and the MCR (whole blood) likewise increased by 15 to 31% (from 295 +/- 23 to 357 +/- 30 l/day/m2), after ACTH or cortisol administration. In vivo and in vitro measurements (at 37 C) of tracer aldosterone concentration in plasma and in red cells showed an increase in distribution to red cells with increasing cortisol concentrations. The results suggest that a fraction of aldosterone is bound in plasma and displaced by cortisol into red cells. There is an increased aldosterone plasma MCR, but unaltered whole blood MCR, since the liver extracts aldosterone almost completely from both plasma and red cells. The increase in cortisol MCR (plasma) results from both an increased splanchnic extraction as plasma binding sites approach saturation and a redistribution into red cells.

Adrenocorticotropic Hormone↗
PubMed1975

Hypocalcemic tetany due to sodium phosphate ingestion in acute renal failure.

The ingestion of a sodium phosphate laxative preparation (Phosphosoda, Fleed) in a patient who had acute renal failure resulted in hypocalcemic tetany primarily due to severe hyperphosphatemia. Hypernatremia and a marked anion gap were present and attributable in part to the sodium phosphate ingestion of this preparation in the presence of renal failure.

Acute Kidney Injury↗
PubMedDate not supplied

Effect of inhibitors of prostaglandin synthesis on induced diuresis in cirrhosis.

The effect of inhibitors of prostaglandin synthesis on diuretic action was examined in patients with ascites due to chronic liver disease and in normal subjects. In patients with ascites, natriuresis after 80 mg i.v. furosemide was reduced 82% by pretreatment with indomethacin. Creatinine clearance was reduced only 16%. These effects were likely due to inhibition of renal prostaglandin synthesis, since urinary prostaglandin E2 fell and there was also reduction in natriuresis with naproxen (52%). The effects were not specific for furosemide since spironolactone-induced natriuresis was also reduced by indomethacin (82%), naproxen (52%), and aspirin (33%). In normal subjects, indomethacin reduced furosemide natriuresis by only 14% while creatinine clearance was not affected. The mechanisms of these drug interactions are uncertain but probably involve renal hemodynamics which appear to be supported importantly by renal prostaglandins in patients with ascites due to liver disease.

Adult↗
PubMedDate not supplied

Immunohistochemical distribution of renal prostaglandin endoperoxide synthase and prostacyclin synthase: diminished endoperoxide synthase in the hepatorenal syndrome.

To evaluate possible causes of the diminished prostaglandin production in advanced hepatorenal syndrome, prostaglandin endoperoxide synthase and prostacyclin synthase were localized and semiquantitated by immunofluorescence in postmortem, biopsy and nephrectomy renal tissues. In normal kidneys, antiprostacyclin synthase serum caused intense staining in peritubular capillaries, in the adjacent renal interstitial cells and in glomerular mesangial regions. Antiprostaglandin endoperoxide synthase serum caused staining of collecting duct epithelial cells, cells of the thin ascending limb and possibly glomerular mesangial cells. Prostacyclin synthase-positive staining was graded 5+ (scale of 0+ to 5+) in all kidney samples. Medullary collecting tubule prostaglandin endoperoxide synthase-positive staining was graded 4+ or 5+ in kidney samples from patients with acute tubular necrosis or acute tubulointerstitial nephritis and from patients with liver failure without the hepatorenal syndrome. However, prostaglandin endoperoxide synthase-positive staining was markedly diminished or absent (average 1+) in patients with the hepatorenal syndrome. These data suggest that loss of the medullary prostaglandin endoperoxide synthase is the cause of diminished urinary prostaglandin E2 excretion in the hepatorenal syndrome.

Adult↗