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Biomedical subjects

R G Luke

Publications and source records attributed to R G Luke.

At least 127 records · Page 7Linked to original sources
PubMed1978

Importance of chloride for acute inhibition of renin by sodium chloride.

To evaluate the contribution of chloride to acute renin inhibition by sodium chloride, plasma renin activity (PRA) was measured before and after peripheral venous infusion of NaCl, NaHCO3, NaBr, NaNO3, lysine monohydrochloride, or lysine glutamate in NaCl-deprived rats. In contrast to controls and animals infused with other sodium salts, PRA decreased (P less than 0.01) after infusion with NaCl [from 28.3 +/- 2.8 to 13.3 +/- 1.8 ng/ml per h (SE)] and NaBr (from 40.6 +/- 6.2 to 21.8 +/- 3.9 ng/ml per h), and renal tubular halide reabsorption increased (P less than 0.05). Arterial pressure, plasma volume, inulin clearance, net sodium balance, serum Na+ and K+, and pH were not different among sodium-loaded groups. PRA was also suppressed (P less than 0.01) by infusion with lysine monohydrochloride (from 51.6 +/- 5.4 to 32.4 +/- 5.1 ng/ml per h) but not with lysine glutamate. These results suggest that inhibition of renin by sodium is dependent on an intrarenal effect of chloride. During infusion with sodium salts which suppressed renin, negative free water clearance (TcH2O) increased, whereas infusion with sodium salts that did not inhibit renin resulted in either no change or decreased TcH2O. The association of renin inhibition and increased TcH2O indirectly supports the hypothesis that renin suppression by chloride is related to the magnitude of absorptive chloride transport in the thick ascending limb of the loop of Henle.

Amino Acids↗
PubMed1978

A possible relationship between Henoch-Schonlein syndrome and IgA nephropathy (Berger's disease). An illustrative case.

A 29-year-old white male with the Henoch-Schonlein syndrome and rapidly progressive glomerulonephritis received a kidney transplant. Postransplant, a glomerulonephritis histologically and immunologically indistinguishable from IgA nephropathy (Berger's disease) developed in the absence of any extrarenal manifestations of the Henoch-Schonlein syndrome. A possible pathogenetic interrelationship between these two diseases is discussed.

Adult↗
PubMed1978

The effects of amphotericin B therapy on the intrarenal vasculature and renal tubules in man. A study of biopsies by light, electron and immunofluorescence microscopy.

Renal morphology was studied by light and electron microscopy in 10 patients after 25 mg/kg body weight of amphotericin B as part of a controlled study designed to evaluate the possible protective effects of mannitol against the nephrotoxicity of amphotericin B. Five patients received amphotericin B 1 mg/kg body weight every other day and five received amphotericin B and mannitol 1 g/kg body weight in the infusion. Small arterial and arteriolar changes were present in all biopsies and were characterized by focal vacuolization of medial smooth muscle cells. Electron microscopy suggested formation of these vacuoles by fusion of dilated endoplasmic reticulum. A few small vacuoles were also seen in renal biopsies of age matched patients who did not receive amphotericin B. Vacuoles in biopsies of the amphotericin treated patients were considerably larger (P less than 0.001) and much more numerous (P less than 0.001) than in controls. It is hypothesized that the vacuoles in the amphotericin B treated group represent the morphologic effect of intrarenal vasoconstriction caused by amphotericin B therapy. Nephrocalcinosis was observed in all biopsies and appeared to originate by precipitation of calcium salts in tubular casts.

Adult↗
PubMed1977

Natriuresis in rats acutely depleted of chloride.

1. Acute chloride depletion, without sodium depletion, was produced in rats by a single exchange peritoneal dialysis against sodium bicarbonate solution. Blood volume was restored after dialysis by infusion of salt-free albumin, and exogenous deoxycorticosterone and antidiuretic hormone were given. 2. Clearance studies in the period (3 h) after dialysis revealed no difference in the glomerular filtration rate or in the filtered sodium load between experimental and control rats but urinary sodium concentrations and absolute and fractional sodium excretion were significantly higher in the chloride-depleted group. 3. There was also a significant kaliuresis, increased urinary flow rate and diminished free water reabsorption. Urinary bicarbonate excretion increased to a variable degree but the major rise in anion excretion was 'unmeasured' (Na+ + K+ - [Cl- + HCO3- + PO4(3-)]). 4. It is postulated that chloride depletion imposes limitations on sodium reabsorption in the ascending limb of the loop of Henle.

Animals↗
PubMed1977

Effects of calcium on renin and aldosterone in the rat.

CaCl2 suppresses the plasma renin activity (PRA) response to Na+ deprivation in the rat. The purpose of the present study is:1) to determine if the effect of Ca2+ on PRA is modified by the anion delivered with Ca2+, and 2) to evaluate the effect of Ca2+ loading on aldosterone production. PRA and in vitro aldosterone production by adrenal quarters were measured after a 7-day balance study. On a low Na+ diet, PRA of animals drinking 1% CaCl2 (13.1 ng/ml per h +/- 1.3 SE), but not of animals drinking 1% calcium gluconate, was suppressed (P less than 0.05) compared to that of water-drinking controls (20.9 ng/ml per h +/- 2.1 SE). Aldosterone production of calcium gluconate and CaCl2-loaded animals was greater than that of controls (P less than 0.01). K+ balance of CaCl2 and calcium gluconate-drinking animals was more positive than that of controls (P less than 0.05). In conclusion, inhibition of PRA by CaCl2 but not by calcium gluconate indicates that the effect of Ca2+ on PRA is modified by the accompanying anion. Both CaCl2 and calcium gluconate stimulate aldosterone production, independent of changes in PRA, possibly due to an effect of Ca2+ on K+ balance.

Adrenal Glands↗
PubMed1977

Effect of volume expansion with NaCl or NaHCO3 on nephron fluid and Cl transport.

To assess the influence of plasma anions on nephron fluid and chloride transport following volume expansion (VE), rats were studied by micropuncture technique during hydropenia and after VE with NaCl (CVE) or NaHCO3 (BVE). VE with either solution produced increments in plasma volume, SNGFR, and fractional sodium excretion (FENa), and decrements in proximal and distal TF/P inulin ratio which were not different. The proximal transepithelial chloride ratio decreased similarly in CVE (from 1.34 to 1.16) and BVE (from 1.32 to 1.17). Following VE, proximal fractional Cl reabsorption decreased similarly in both CVE (-5.9%) and BVE (-7.4%). Early distal fractional Cl reabsorption also was decreased in CVE (-12%) but not in BVE (-1%). Fractional chloride excretion increased in CVE but not in BVE. Therefore, following VE plasma anion composition did not significantly modify either fluid reabsorption in proximal tubule or loop of Henle or urinary Na excretion. The fraction of sodium reabsorbed with chloride in the proximal tubule increased, and Cl conservation, primarily within the loop of Henle, can be maintained despite marked natriuresis.

Animals↗
PubMed1977

Insulin resistance in uremia: amino acid metabolism.

After infusion of 250 ml of essential L-amino acids, plasma levels of alpha-amino nitrogen (alpha-AN2) in six chronic renal failure (CRF) patients were not different from those in six carefully matched control (CON) subjects. Plasma insulin increments increased significantly within both groups but were higher in the CRF group (p less than 0.05 at 40 min, p less than 0.005 at 55 min). Growth hormone levels were also higher in the CRF group. Previous studies have shown delayed clearance of plasma alpha-AN2 after casein hydrolysate infusion, despite similarly increased insulin and growth hormone levels in CRF patients. We conclude that essential amino acids are probably more easily metabolized than casein hydrolysate in uremic subjects, but that normal metabolism occurs at the expense of higher plasma levels of insulin and growth hormone.

Adult↗
PubMed1977

'Hyperacute rejection' due to perfusion injury.

Two kidneys were harvested from a cadaver donor and subjected to pulsatile perfusion in an identical fashion with a perfusate which was free of cytotoxic antibody. Classical 'hyperacute rejection' occurred in the right kidney when transplanted into a male patient with no previous blood transfusion or transplants, and repeatedly negative tests for cytotoxic antibody. The left kidney was not transplanted and was examined by light, electron, and immunofluorescence microscopy as was the immediately removed, transplanted kidney. Despite the absence of any immunological pathogenetic mechanism in the non-transplanted kidney, virtually identical changes of 'hyperacute rejection' were seen in both kidneys. Thus,even technically satisfactory perfusion may cause a syndrome of 'hyperacute graft failure' secondary to non-immunologically mediated perfusion injury.

Adult↗
PubMed1977

Effect of calcium gluconate infusion on renin in the dog.

We have previously reported that infusion of CaCl2 into the renal artery of the dog inhibits renin release. To evaluate the possible importance of the anion delivered with calcium, similar experiments were performed in 10 dogs with equivalent amounts of calcium gluconate (0.3 mg. of Ca++ per kilogram of body weight per minute). The experiment consisted of three successive 15 minute control periods, followed by three 15 minute calcium gluconate infusion periods and two 15 minute recovery periods. During calcium gluconate infusion, mean serum Ca++, and ECa++, ENa+, and EFNa+ from the infuses kidney increased (p less than 0.005). Systolic blood pressure (142 mm. Hg +/- 8S.E.), renal blood flow (137 ml. per minute +/- 11 S.E.), creatinine clearance, and aldosterone excretion (12.0 ng. per 15 minute +/- 1.5 S.E.) did not change (p less than 0.3). Renal venous PRA (28.4 ng. per millileter per hour +/- 7.5 S.E.) decreased (p less than 0.014). The per cent decrease of PRA correlated (r = -0.70) with the per cent increase EFNa+ (p less than 0.001). Calcium gluconate had a lesser (p less than 0.01) inhibitory effect on renin than CaCl2, despite greater excretion of Ca++ and Na++ during calcium gluconate infusion. Taken together, the results indicate that Ca++ inhibits renin release, although the extent of the inhibition is modified by the anion accompanying Ca++. The effect of Ca++ on renin may be mediated by NaCl transport across the macula densa.

Animals↗
PubMed1976

Goodpasture's syndrome in a patient with the Nail-Patella syndrome.

A patient with the nail-patella syndrome in whom end-stage renal failuure developed as the result of Goodpasture's syndrome is described. Lesions characteristic of both rare diseases were seen on renal morphology. It is postulated that the glomerular membrane alteration of the nail-patella syndrome predisposed to the development of antiglomerular basement membrane antibody and hence Goodpasture's syndrome. A review of the incidence of renal failure in the nail-patella syndrome suggests that renal involvement can no longer be regarded as benign and that immune mechanisms may be related to progressive renal disease in some cases.

Adolescent↗
PubMed1976

Chloride depletion and hypochloraemia as a cause of renal sodium and water loss in the rat.

1. To study the effects of chloride depletion, without sodium depletion or change in plasma tonicity, on renal excretion of sodium and water, a single exchange peritoneal dialysis was performed in rats against a solution of glucose (15 g/1) containing either NaCl (150 mmol/l, control) or NaHCO3 (150 mmol/l, experimental); KHCO3 (4mmol/l)was added to both solutions. All rats were prepared before dialysis by a low NaCl diet for 10 days. 2. Peritoneal dialysis against NAHCO3 consistently produced a negative sodium and water balance compared with dialysis against NaCl. Despite this, subsequent electrolyte balance for 3 days showed that chloride-depleted rats excreted significantly more sodium and water and had a reduced urinary osmolality as compared with control animals. Increased sodium and water loss were unexplained by osmotic or bicarbonate diuresis. Kaliuresis was seen in the chloride-depleted rats but muscle potassium was not significantly depressed. 3. With sodium and water loss and continued renal chloride conservation, plasma chloride rose on the average from 88 mmol/l after dialysis against NaHCO3 to 100 mmol/l (control 104 mmol/l) at 72 h. Concomitant with this increase in plasma [C1-], on the third day after dialysis, during hydropenia, urinary osmolality and papillary [Na+] were not different from control cencentrations. 4. It is postulated that chloride depletion and/or hypochloraemia leads to diminished chloride transport in the loop of Henle and that this causes reduced sodium transport into the medulla, impaired concentration ability and inappropriate urinary sodium loss.

Animals↗