Life-long food restriction prevents renal membrane lipid deposition and lowers renal work in rats.

Renal cortical brush-border (BBM), basolateral membrane (BLM), and medullary plasma membrane (mPM) preparations were analyzed to assess the effects of life-long food restriction in aged rats on membrane lipid content. Young male Fischer 344 x Brown-Norway F1 rats consumed food ad libitum (young AL) or were food-restricted (FR, 60% of AL consumption) for either 6 weeks (young FR) or until the age of 30 months old (old FR). Senescent FR rats had 50 per cent decreases in fractional excretion of Na and K (p < 0.

Exchange transfusion in severe falciparum malaria: a simple method modified from hemodialysis circuit.

We set up a simple extracorporeal circuit, modified from the extracorporeal method generally used in conventional hemodialysis, for exchange transfusion. Temporary vascular access was used in exchange transfusion for both draining the infected blood and infusion of the freshly non-infected blood. This method of exchange transfusion was performed in 3 severe complicated falciparum malaria patients who had a percentage of parasitemia of 80, 40, and 35.

Pharmacokinetic studies of cyclosporin in Thai kidney transplantation patients.

Pharmacokinetic studies were performed in 10 Thai patients with kidney transplantation who received microemulsion formulation (Neoral) of cyclosporin A (CsA) twice daily. No agents having pharmacokinetic effect on CsA had been used in these patients. The mean values of 12-h AUC (area under the concentration-blood curve) were 4603.

Potassium depletion: renal membrane lipid metabolism and Na/H exchanger abundance in aged F344 x BNF1 rats.

Potassium depletion (-K) is a common electrolyte abnormality in elderly humans, occurring after diuretic use or poor oral intake. We hypothesized that aging would result in an increase in renal membrane lipid metabolism in both control and -K, and that the Na/H exchanger's protein abundance to -K would be blunted. Young and senescent non-obese male Fisher 344 x Brown-Norway F1 rats (F344 x BNF1) were fed either a normal or a K-deficient diet for 7 days.

Age-related changes in renal function, membrane protein metabolism, and Na,K-ATPase activity and abundance in hypokalemic F344 x BNF(1) rats.

Background: Potassium depletion is a common electrolyte abnormality in elderly humans, usually as a consequence of diuretic use or poor oral intake. Hypokalemia is associated with a number of changes in renal function and an increase in some renal membrane transporters; its growth-promoting effect in young animals is well known. With aging, the renal adaptation to a number of challenges is often diminished.

Food restriction beneficially affects renal transport and cortical membrane lipid content in rats.

Food restriction (FR) exerts a variety of beneficial effects and may prolong life in both humans and animals. However, studies of its effects on the cortical brush border membrane (BBM) and basolateral membrane (BLM) lipid concentration, which may be pertinent to renal function, have not been reported in detail. We hypothesized that FR would decrease renal work and lower renal membrane lipid concentration.

Environmental distal renal tubular acidosis in Thailand: an enigma.

Distal renal tubular acidosis is a common health problem in northeastern Thailand, with the population background of the low potassium intake, low urine citrate, and decreased red blood cell Na-K adenosine triphosphatase (ATPase) activity and the environment of the high soil vanadium. The disease is usually seen in the people with low socioeconomic status in summer. The patients have decreased gastric acidity and low urine potassium.

Falciparum malaria and the kidney: a model of inflammation.

Renal and renal-related disorders commonly occur in infection with Plasmodium falciparum, which can cause fluid and electrolyte disorders, glomerulonephritis, and acute renal failure (ARF). It appears that ARF and other life-threatening complications in falciparum malaria are not directly caused by the parasite itself but are the result of interaction of mechanical, immunologic, and humoral components. P.

Hepatitis virus and kidney.

Hepatitis A, B and C viruses are major causes of viral hepatitis in human. These infectious agents not only damage liver parenchyma but can also affect renal parenchyma. Hepatitis A virus could produce acute renal failure in a similar fashion to hepatorenal syndrome.

Studies on the mechanism of trimethoprim-induced hyperkalemia.

We examined the effects of trimethoprim (TMP) on metabolic parameters and renal ATPases in rats after a 90 minute infusion (9.6 mg/hr/kg body wt, i.v.

Biochemical mechanisms and regulation of hydrogen transport in renal tubules.

In normal humans, blood pH and bicarbonate concentration are maintained within a very narrow range despite wide variations in dietary intake. The mechanisms involved in the chronic regulation of acid-base homeostasis relate to the kidney in general, and specifically to changes in membrane-bound ATPases and exchangers. This review summarizes some of the data regarding the Na/H exchanger, the H-ATPase and its interaction with Na,K-ATPase and the Ca-ATPase and Ca/H exchanger in renal tissue.

Renal ATPases twenty-four hours after uninephrectomy: the role of IGF-1.

We studied the effect of 24 h of uninephrectomy and somatostatin analogue, an inhibitor of growth hormone secretion, in microdissected nephron segment H-ATPase, H-K ATPase and Na-K ATPase activities. Systemic acid-base status, plasma and tissue electrolytes, and aldosterone levels in the uninephrectomized rats were similar to controls. Uninephrectomy increased fractional sodium, potassium, and bicarbonate excretion (p < 0.

Insights into the biochemical mechanism of maleic acid-induced Fanconi syndrome.

Maleic acid administration is known to produce the Fanconi syndrome, although the biochemical mechanism is incompletely understood. In this study the effect of a single injection of maleic acid (50 mg/kg body wt, i.v.

Diseases of renal adenosine triphosphatase.

Most renal transport is a primary or secondary result of the action of one of three membrane bound ion translocating ATPase pumps. The proximal tubule mechanisms for the reabsorption of salt, volume, organic compounds, phosphate, and most bicarbonate reabsorption depend upon the generation and maintenance of a low intracellular sodium concentration by the basolateral membrane Na-K-ATPase pump. The reabsorption of fluid and salt in the loop of Henle is similarly dependent on the energy provided by Na-K-ATPase activity.

Effect of respiratory acidosis and respiratory alkalosis on renal transport enzymes.

We studied the effect of respiratory acidosis and respiratory alkalosis on acid-base composition and on microdissected renal adenosinetriphosphatase (ATPase) enzymes. Rats were subjected to hypercapnia or hypocapnia of 6, 24, and 72 h duration. After 6 h of hypercapnia, collecting tubule (CT) ATPases were not changed.

Metabolic acidosis and bone disease.

Bone is the largest repository base in the body. Prolonged acid retention requires continuous buffering of acid if the organism is to survive. This paper discusses the role of bone buffering under both normal and altered conditions of acid-base homeostasis.

H-K-ATPase in distal renal tubular acidosis: urinary tract obstruction, lithium, and amiloride.

In previous studies we suggested that urinary tract obstruction and chronic administration of lithium or amiloride were models of "voltage-dependent" distal renal tubular acidosis (DRTA). Subsequently, differences among these three models suggested that the pathogenesis was far more complex than we originally proposed. A recent study showed that H-adenosinetriphosphatase (H-ATPase) activity was decreased in all three experimental models.

Stimulation of basolateral Na(+)-HCO3- cotransporter by angiotensin II in rabbit renal cortex.

Angiotensin (ANG) II is now recognized as a powerful direct controller of Na+ reabsorption in the proximal convoluted tubule, a property that predominantly reflects stimulation of the transepithelial NaHCO3 flux. Numerous studies have established that this effect of ANG II represents stimulation of the apical Na+/H+ exchanger, but a single microperfusion study has also suggested direct stimulation of the basolateral Na(+)-HCO3- cotransporter. We have carried out studies in basolateral membrane vesicles from rabbit renal cortex to examine directly whether ANG II exerts an independent effect on the Na(+)-HCO3- cotransporter.

Regulation of collecting tubule adenosine triphosphatases by aldosterone and potassium.

To examine the precise role of potassium and aldosterone on acid-base composition and on collecting tubule ATPases, glucocorticoid-replete adrenalectomized rats were replaced with zero, physiological, or pharmacological doses of aldosterone and were fed varying potassium diets to produce hypokalemia, normokalemia, or hyperkalemia. Radiochemical measurement of ATPase activities showed that collecting tubule H/K-ATPase changed inversely with potassium and not with aldosterone whereas H-ATPase changed directly with aldosterone but not with potassium. When both enzymes changed in the same direction, alterations in acid-base composition were profound; however, when these two acidifying enzymes changed in opposite directions or when only one enzyme changed, the effect on acid-base balance was modest.

Effect of furosemide-induced hypokalemic metabolic alkalosis on renal transport enzymes.

Hypokalemic metabolic alkalosis is one of the most common complications of chronic furosemide administration. In this study we examined acid-base composition and ATPase enzyme activities in medullary thick ascending limb of Henle's loop (MTAL) and collecting tubule (CCT and MCT) after seven days of chronic furosemide therapy. All of the studies were conducted in adrenal intact (AI) rats or in adrenalectomized (ADX) glucocorticoid replete rats replaced with a physiological dose of aldosterone (Aldo).

Endothelin-1 stimulates the Na+/H+ and Na+/HCO3- transporters in rabbit renal cortex.

Endothelin-1 (ET-1) is the most potent endogenous vasoconstrictor identified to date, raising the strong possibility of its involvement in the pathogenesis of systemic hypertension. Whether ET-1 exerts a direct stimulating effect on sodium reabsorption in the renal proximal convoluted tubule, the dominant locus of sodium reabsorption in the nephron, is currently unknown. Such an effect would suggest yet another mechanism by which ET-1 might mediate systemic hypertension.

Identification of urinary metabolites and quantitative measurement of creatinine by a proton nuclear magnetic resonance spectrometry.

1H-NMR spectra of 60 human urine specimens were recorded without pretreatment by a JEOL FX 90 Q spectrometer operating at 89.55 MHz. The signals of the methyl protons of creatinine (3.