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At least 19 recordsLinked to original sources
PubMed1979

Morphometric observations on the kidney of the camel, Camelus dromedarius.

Morphometric analysis of the kidney of the camel was carried out on gross slices and histological sections using standard morphometric methods. The renal cortex occupied about 50% by volume of the kidney, and the ratio of the thickness of the medulla to that of the cortex was about 4:1. The relative thickness of the medulla was about 7.89. This parameter is an indicator of the lengths of the loops of Henle and vasa recta, and, according to the countercurrent theory, is consequently an indicator of the ability of the kidney to concentrate urine. In each kidney the volume and surface area of the cortical tubules and the number of glomeruli were determined and compared with these parameters in some other mammals. In addition the architectures of the renal pelvis and medulla and their significance in relation to the excretion of hypertonic urine were discussed. It was concluded that the kidney of the camel possesses the anatomical requisites for the production of hypertonic urine.

Animals↗
PubMed1976

[Tubular response to antidiuretic plasma activity in the transplanted kidney (author's transl)].

Reabsorption of osmotically free water (TmcH2O) was studied in 10 patients after renal transplantation. A rising or constant free water reabsorption was observed under hydropenia and increasing tubular solute load. These findings suggest that in the transplanted kidney the functioning nephrons respond in a normal way to plasma ADH-activity. The excretion of plasma-hypotonic urine reflects decreased antidiuretic activity as in overhydration rather than tubular unresponsiveness to ADH. The excretion of plasma-hypertonic urine indicates tubular reabsorption of osmotically free water due to ADH, and this in general rules out overhydration. Daily estimation of urinary and plasma osmolality will be useful in judging the actual state of hydration after renal transplantation.

Blood↗
PubMed1975

Renal tubular function in patients on long-term lithium therapy.

The authors conducted a study in which 10 patients with recurrent affective disorders who responded completely to long-term lithium therapy but who were otherwise unselected were tested for renal tubular concentrating and acidification ability. Despite frequent symptoms of thirst, polyuria, and nocturia, all patients were able to concentrate urine normally and all showed normal renal tubular acidification ability. A significant correlation was found between erythrocyte lithium concentration and maximum urinary osmolality.

Humans↗
PubMed1979

Urinary concentrating ability during dehydration in the absence of vasopressin.

Despite the apparent absence of vasopressin (ADH), Brattleboro homozygotes [diabetes insipidus (DI) rats] can concentrate their urine when deprived of drinking water. Since other investigators have shown that reducing glomerular filtration rate (GFR) improves the concentrating ability of water-loaded dogs, the present studies were undertaken to quantify the magnitude and time course of changes in GFR during dehydration. Clearance experiments were performed in 10 conscious DI rats before and following 3, 6, 9, 12, 15, and 24 h of dehydration. Urine osmolality increased from 155.0 +/- 12.6 (SE) to 696.7 +/- 8.4 mosmol/kg H2O after 24 h. GFR averaged 984.3 +/- 79.6 microliters . min-1 . 100 g body wt-1 in the control phase, fell to about 80% of this value over the first 12 h of dehydration, and then declined to 27% at 24 h. The rats lost 20% of their body weight over the 24 h. The osmolality of the papillary tip averaged 896 +/- 44 mosmol/kg H2O at 24 h compared to a control value of 493 +/- 28. The lack of osmotic equilibration between urine and papillary interstitium suggests that dehydration did not appreciably increase the water permeability of the distal nephron. These experiments clearly show a progressive decline in GFR as urine becomes concentrated during dehydration in the absence of ADH; these events may or may not be causally related.

Animals↗
PubMed1975

Reversible renal concentrating defect in shock.

The loss of renal concentrating power in haemorrhagic shock is reversible upon correction of the shock state. Shock resulting from acute hypovolaemia leads to the following sequence of events: (1) diminished renal blood-flow; (2) decreased superficial cortical nephron perfusion; (3) continued juxtamedullary nephron perfusion; (4) enhanced proximal reabsorption of Na, Cl, and H23; (5) decreased delivery of these ions to the ascending limb, which results in diminished hypertonicity of the medullary interstitium. This hypotonicity is worsened by the "washout" effect on the interstitial hypertonicity caused by continued perfusion of the juxtamedullary vasa recta which results in (6) diminished renal concentrating capacity due to elimination of medullary hypertonicity. Replenishing blood-loss and correcting the hypovolaemic state "regenerates" the hypertonic renal medullary interstitium by (a) diminishing proximal reabsorption and allowing presentation of greater quantities of Na and Cl to the ascending-limb "pump", (b) restoring superficial cortical nephron perfusion, thereby decreasing juxtamedullary perfusion and in this manner eliminating medullary "washout".

Animals↗
PubMed1976

Some effects of ammonium salts on renal histology and function in the dog.

NH4Cl was infused into the left renal artery of anesthetized dogs at 50-125 mum/kg/min for up to 110 min. Renal blood flow declined early then increased to supra-control levels during infusion. Kidneys perfused at 125 mum/kg/min for 90 min showed patchy to confluent mixtures of cortical necrosis and tubular necrosis. Experimental kidneys invariably showed lower urine osmolality than contralateral controls 48 h after perfusion. Kidneys with necrosis showed depressed creatinine clearance as well. Renal artery infusion of NH4 acetate or intravenous infusion of NaHCO3 during arterial infusion of NH4Cl prevented significant acidosis and caused minimal histological changes, but depression of urine osmolality was not prevented. It is concluded that renal ammonium concentrations up to 40 mum/liter for 90 min does not cause tubular necrosis but does impair urine concentration. Severe tissue damage followed renal exposure to high ammonium concentrations in the presence of metabolic or renal acidosis.

Ammonia↗
PubMed1977

Antidiuretic hormone and the distribution of renal cortical blood flow.

The radioactive microsphere method was used to study the distribution of cortical blood flow in anesthetized dogs during water diuresis and during antidiuresis. Infusion of antidiuretic hormone (ADH) at rates ranging from 0.33 to 0.5 mU/kg-min into dogs previously volume expanded with 3% dextrose resulted in an increase in urinary osmolality and a significant increase in fractional flow in the inner cortex. Mean arterial pressure, glomerular filtration rate, and renal plasma flow were unaltered by the infusion of ADH at these doses, suggesting that absolute, as well as fractional, blood flow to the inner cortex increased in response to ADH. In three additional experiments, termination of an infusion of ADH in hydropenic dogs and subsequent induction of water diuresis was accompanied by a shift in fractional cortical blood flow away from the inner cortex. The redistribution of cortical blood flow in response to ADH at a time when the kidney is producing a more concentrated urine supports the hypothesis that this vascular effect of ADH may have functional significance in the urinary concentration ability of the kidney.

Animals↗
PubMed1978

Mannitol osmolar clearance in diabetes insipidus of children.

A modified technique of amnnitol-induced diuresis is described, in order to assess renal concentrating ability in infants and children. The infusion of 10% mannitol in 0.9% saline avoided the hypertonic saline overload and the fluid restriction period, both badly tolerated by infants and small children. In a control group of children aged from two months to seven years, the values of T(H2O) plotted against C(OSM) allowed to calculate the adjustment curve y=0.80x0.75, r=0.98 (p is less than 0.0001). In six patients with pituitary diabetes insipidus (PDI), the test was used in order to quantify the degree of ADH deficiency and evaluate the carbamazepine and clofibrate effect, in the renal concentrating mechanism. The test was tolerated perfectly in every case, obtaining qualitative and quantitative data and avoiding the hyponatremia and hypokalemia produced by the mannitol.

Carbamazepine↗
PubMed1977

Renal function testing: differentiation between a nephrotoxic agent and diuretic drugs.

Preliminary studies indicate that it may be possible to differentiate the effects of a nephrotoxic substance from those of diuretic agents by the measurement of both urine and plasma osmolarity. The nephrotoxic substance, mercuric chloride, decreases urinary osmolality and increases plasma or serum osmolality. The diuretic agents, at exceedingly high dosages, may show a dose-related decrease in urine osmolality. However, serum osmolality either remains unchanged or is only slightly lowered. This difference in the serum response of animals treated with a nephrotoxin or diuretic agents may allow for the differentiation in toxicological studies.

Acetazolamide↗