Increase In Renal Tubular Reabsorption Research Articles

A comparative study on obese and non-obese for evaluating the risk of hypertension

Obesity-associated arterial hypertension is characterized by stimulation of the sympathetic nervous system, activation of the renin-angiotensin system (RAS) and sodium retention, among other abnormalities. Stimulation of the sympathetic nervous system has been considered to have an important function in the pathogenesis of obesity-related hypertension. During the early phases of obesity, primary sodium retention exists as a result of increase in renal tubular reabsorption. Plasma renin activity, angiotensinogen, angiotensin II and aldosterone values display significant increase during obesity. Leptin and other neuropeptides are possible links between obesity and the development of hypertension. Obesity should be considered as a chronic medical condition, which is likely to require long-term treatment. Understanding of the mechanisms associated with obesity-related hypertension is essential for successful treatment strategies.

Alterations in serum uric acid values in a sample of Nigerian pregnant women.

Introduction: Serum uric acid level is an important prognostic variable in pregnancy as subjects with preeclampsia have elevated serum uric acid levels. Methods: The concentrations of serum uric acid were investigated in 100 women of which 75 were pregnant women and categorized into 3 groups of 25 each, based on their trimesters of pregnancy and 25 non-pregnant women, which served as control. Results: In the first trimester, the mean values of uric acid were 122 μmol/L with a decrease in the levels of uric acid when compared with the control levels of 308 μmol/L (p<0.05). In the second trimester, the values of uric acid were 199umol/l with a significant (p<0.05) decrease in the levels of uric acid when compared with the controls. In the third trimester of pregnancy, the values of uric acid were 360 μmol/L. There was a significant (p<0.05) increase in the level of uric acid when compared with the controls. Conclusion: The progressive increase in the levels of uric acid through the trimesters of pregnancy suggests an impairment in uric acid excretion, may be with concomitant increase in renal tubular re-absorption of uric acid, thereby leading to hyperuricaemia.

Mechanisms of obesity-induced hypertension

The relationship between obesity and hypertension is well established both in children and adults. The mechanisms through which obesity directly causes hypertension are still an area of research. Activation of the sympathetic nervous system has been considered to have an important function in the pathogenesis of obesity-related hypertension. The arterial-pressure control mechanism of diuresis and natriuresis, according to the principle of infinite feedback gain, seems to be shifted toward higher blood-pressure levels in obese individuals. During the early phases of obesity, primary sodium retention exists as a result of increase in renal tubular reabsorption. Extracellular-fluid volume is expanded and the kidney-fluid apparatus is resetted to a hypertensive level, consistent with a model of hypertension because of volume overload. Plasma renin activity, angiotensinogen, angiotensin II and aldosterone values display significant increase during obesity. Insulin resistance and inflammation may promote an altered profile of vascular function and consequently hypertension. Leptin and other neuropeptides are possible links between obesity and the development of hypertension. Obesity should be considered as a chronic medical condition, which is likely to require long-term treatment. Understanding of the mechanisms associated with obesity-related hypertension is essential for successful treatment strategies.

Role of bone and kidney in parathyroid hormone-related peptide-induced hypercalcemia in rats

A protein responsible for the biochemical syndrome similar to primary hyperparathyroidism associated with certain tumors has been recently characterized and its effects at the level of bone and kidney reported. However, the relative role of tubular reabsorption of calcium (Ca) and bone resorption in the pathogenesis of hypercalcemia induced by this factor is still debated. We investigated the effects of a synthetic amino-terminal fragment of parathyroid hormone-related protein [PTHrP-(1-34)] administered chronically by intraperitoneal osmotic minipumps in thyroparathyroidectomized (TPTX) rats. Clearance studies performed on day 6 of treatment after a 24 h fast revealed an increase in renal tubular reabsorption of Ca and a decrease in renal tubular reabsorption of phosphate (Pi), accompanied by an increase in cAMP excretion. PTHrP-(1-34) (90 pmol/h) stimulated bone resorption as evaluated by an increment in fasting urinary Ca excretion. Although the bone resorption inhibitor aminopropylidene diphosphonate fully corrected urinary Ca excretion and reduced plasma Ca from 3.04 +/- 0.07 to 2.44 +/- 0.21 mM (p less than 0.05), this latter value remained considerably higher than in TPTX control rats (1.54 +/- 0.12 mM, p less than 0.01). In contrast, when the agent WR-2721, which is known to decrease the renal tubular reabsorption of Ca by a PTH-independent mechanism, was given, a further drop in plasma Ca and an increase in urinary Ca excretion were observed. These findings are similar to those found in animals implanted with the hypercalcemic Leydig cell tumor.(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanism of malignant hypercalcaemia in carcinoma of the breast.

To investigate the mechanisms of hypercalcaemia in carcinoma of the breast, 22 patients with hypercalcaemia due to metastatic carcinoma were studied and the findings compared with those obtained in normal subjects and patients with benign and malignant breast disease without hypercalcaemia. As expected, patients with metastases of bone showed biochemical evidence of increased bone resorption. Whereas all patients with hypercalcaemia had skeletal metastases, not all patients with skeletal metastases had hypercalcaemia despite considerable degrees of bone resorption. The presence of hypercalcaemia was associated with a significant increase in renal tubular reabsorption of calcium (p less than 0.001) and decreased reabsorption of phosphate (p less than 0.001) despite adequate rehydration of patients. These studies suggest that increased renal tubular reabsorption of calcium, possibly mediated by a humoral factor with activity similar to that of parathyroid hormone, contributes appreciably to the hypercalcaemia of malignant breast disease.

Effect of a thiazide diuretic (Bendroflumethiazide) on parathyroid function in humans

It is well known that treatment with thiazides reduces urinary calcium excretion in normal subjects as well as in patients with idiopathic hypercalciuria (Lamberg & Kuhlbäck 1959, Coe et al. 1973, Goulding et al. 1978, Backman et al. 1979). This reduction results from an increase in renal tubular reabsorption of calcium, considered to be due to a direct action of thiazides on the kidneys (Goulding et al. 1978). As to the effect of thiazides on parathyroid function, the data reported so far (Coe et al. 1973, Zerwekh & Pak 1980) are both limited and conflicting. It was therefore considered worthwhile to study systematically the effect of a thiazide (bendroflumethiazide) on parathyroid function in humans, as estimated from measurements of nephrogenous cAMP. Our results are presented in Table I. Twelve subjects (cases 1–12) were normal controls. Of the remaining cases, 13 (cases 13–25) were patients with absorptive idiopathic

Familial Benign Hypercalcaemia: STUDY OF A LARGE FAMILY

Twenty-seven hypercalcaemic subjects were identified in three generations of a family. There were no clinical complications of chronic hypercalcaemia, but five had had parathyroid surgery which was unsuccessful in four. Twenty of the twenty-seven subjects were compared with twenty-four normocalcaemic controls from the same family and the findings were also compared with those from forty patients with surgically proven primary hyperparathyroidism. The relation between the serum and urinary calcium levels was studied by means of an oral calcium loading test. The ratio of calcium clearance to creatinine clearance was normal in this family (but elevated in the patients with primary hyperparathyroidism) and the concentration of parathyroid hormone was normal, as was the total urinary excretion of cyclic AMP. Thus, there was no evidence of either suppressed or increased parathyroid activity in this familial condition. Basal urinary calcium excretion was normal under steady-state conditions indicating that the hypercalcaemia could not be attributed to either increased bone resorption or increased calcium absorption from the gut. In accordance with this, the serum levels of 1,25-dihydroxycholecalciferol were normal. The hypercalcaemia in this condition can be accounted for in full by an increase in renal tubular reabsorption of calcium, and thus differs from that of primary hyperparathyroidism in which there is increased production of calcium from gut and/or bone as well as an increase in renal tubular reabsorption of calcium. Although the serum phosphate and renal tubular reabsorption of phosphate were both low in patients with familial benign hypercalcaemia, they were not as low as in patients with the same degree of hypercalcaemia due to primary hyperparathyroidism. The changes in phosphate transport in familial benign hypercalcaemia could be explained as a secondary effect of the increased filtered load of calcium in the kidney. The tendency towards hypermagnesaemia in our patients, which contrasts with a tendency towards hypomagnesaemia in primary hyperparathyroidism, could also be explained as a secondary effect of the abnormality of renal tubular reabsorption of calcium. Increased renal tubular calcium reabsorption and persistent normal functioning of the parathyroid glands in the face of hypercalcaemia remain the sole definite abnormalities of the syndrome.

Association of hypokalaemia and hypophosphataemia.

A prospective study of 13 patients with hypokalaemia due to a variety of causes demonstrated that six had hypophosphataemia. In 10 patients the plasma inorganic phosphate level rose on correction of the hypokalaemia. Before treatment seven patients had an excessive rate of excretion of phosphate relative to creatinine in the urine. Following correction of the hypokalaemia 11 patients had an increase in renal tubular reabsorption of phosphate relative to creatinine. It is suggested that hypokalaemia may be causally related to the hypophosphataemia, and that in chronic potassium depletion this may affect bone mineralization.

Renal tubular response to aldosterone in normal infants and children with adrenal disorders.

Abstract The renal tubular response to aldosterone was evaluated in 4 normal infants and 7 children with various disorders of the adrenal cortex. An increase in renal tubular sodium reabsorption was demonstrated in all patients with adrenal disease. In one infant with the salt-wasting form of the adrenogenital syndrome studied prior to receiving any hormonal therapy, the response to aldosteixme administration was comparable to that of older, treated children with the adrenogenital syndrome and infants with simple virilizing adrenal hyperplasia and adrenal insufficiency. Three of 4 normal infants failed to show an increase in renal tubular reabsorption of sodium in response to aldosterone administration. This lack of response to aldosterone was interpreted as being a reflection of the effects of a large sodium load on the relatively immature glomerular and tubular functions of the newborn kidney.