Diuresis pattern, plasma vasopressin and blood pressure in healthy elderly persons with nocturia and nocturnal polyuria.
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BACKGROUND: Nocturia, a common symptom in the elderly, is often caused by increased urine production at night. METHODS: The present study comprised 17 men and six women aged 68.1 +/- 4.7 (mean +/- SD) years with nocturia (> or = 2 nocturnal voids) and nocturnal polyuria (nocturnal urinary output of > or = 0.9 mL min(-1)). A physical examination, measurements of recumbent blood pressure after a 15-minute rest, plasma AVP assay at noon and midnight, and urine collection performed during a 24-hour period. RESULTS: The daytime urine output was 1358 +/- 664 mL, and the nocturnal urine output 796 +/- 312 mL. The AVP level was lower at midnight than at noon in 17 persons, and higher at midnight in six persons. Blood pressure was 142.0 +/- 15.7/87.4 +/- 9.1 mmHg. Systolic (but not diastolic) blood pressure increased with decreasing nocturnal plasma AVP. Increasing nocturnal diuresis rate (r2= 0.26; p < 0.01) but not plasma AVP was associated with increasing systolic blood pressure. CONCLUSION: In elderly persons with nocturia and nocturnal polyuria, the plasma AVP is low and does not rise nocturnally. The systolic blood pressure is increased with increasing diuresis but unaffected by plasma AVP. (+info)
Risk factors for the development of lithium-induced polyuria.
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BACKGROUND: Polyuria is common in patients with bipolar disorder treated with lithium. However, the risk factors for polyuria in these patients have not been established. AIMS: To estimate the prevalence of polyuria associated with the use of lithium and to identify additional risk factors. METHOD: A 4-month prospective follow-up study in an out-patient lithium clinic. The 75 participants were asked to provide 24-h urine samples; polyuria was defined as a urine volume greater than 3 litres per 24 h. Risk factors examined included demographic variables, medications and medical comorbidities. RESULTS: The prevalence of polyuria among lithium users was 37%. Concomitant use of serotonergic antidepressants was strongly associated with polyuria (odds ratio 4.25, 95% CI 1.15-15.68) compared with patients not using these agents. CONCLUSIONS: Our data confirm the high prevalence of lithium-induced polyuria. Physicians should be aware that concurrent use of serotonergic antidepressants and lithium significantly enhances the risk of its occurrence. Although limited polyuria is not harmful, it may be troublesome for the patient. In many cases cessation of lithium therapy is not an option because of difficulty in controlling the manic or depressive symptoms. (+info)
An integrative physiological approach to polyuria and hyponatraemia: a 'double-take' on the diagnosis and therapy in a patient with schizophrenia.
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A patient with a history of schizophrenia was brought to the emergency department with extensive self-inflicted soft tissue injuries. Primary polydipsia was evident on admission, because he had a maximally dilute urine, a urine flow rate of 10 ml/min, and hyponatraemia (100 mmol/l). During an imaginary consultation with Professor McCance in which he applied basic principles of integrative physiology and a deductive analysis in quantitative terms, other reasons for the polyuric state were considered. Moreover, based on the very low value for the concentration of urea in plasma (< 0.7 mmol/l, BUN 1 mg /dl), the goals of therapy to prevent osmotic demyelination became evident. Applying this simple approach, a more comprehensive and accurate differential diagnosis, and a plan for therapy to avoid serious complications was compiled. (+info)
Polyuria in paroxysmal tachycardia and paroxysmal atrial flutter and fibrillation.
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When Paul Wood spoke about this to the British Cardiac Society in 1961, we were impressed by the originality of his work on a subject that so many had noticed but failed to investigate. A few months before his death in July 1962, when I asked him if his paper was ready for the journal, he said that he had not yet been able to get all the evidence he hoped for to establish the full explanation. Unfortunately, he had not the time to complete this. I have, therefore, tried to set out as clearly as possible the stage that he had reached. Maurice Campbell (+info)
Compulsive polydipsia with defective renal concentrating capacity.
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Observations are presented on two patients with chronic compulsive polydipsia who showed a relative defect in renal concentrating capacity. After excluding all possible metabolic and renal causes of hyposthenuria and after obtaining normal kidney biopsies, both patients were studied in metabolic balance on a constant diet under the following conditions: (a) dehydration (loss of 3-5% body weight), (b) water loading and response to hypertonic saline, and (c) water loading and response to intravenous vasopressin (Pitressin). Throughout these studies the following parameters were observed: plasma and urine osmolality, glomerular filtration rate (inulin), renal plasma flow (P.A.H.), osmolar clearance and clearance of free water. In both patients the concentration defect was not related to variations in glomerular filtration rate or osmotic load. There was no correlation between the degree of hypoosmolality and the renal concentrating defect. Contrary to reports from other laboratories, restriction of water intake and chronic administration of intramuscular vasopressin did not correct the concentration defect. (+info)
PHENACETIN NEPHROPATHY.
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Four patients who had ingested large amounts of phenacetin-salicylate medications were studied during a 12-month period. Renal failure had progressed slowly over a number of years. All patients took the drug because of psychogenic headache. Considerable skill was required to elicit the history of drug habituation. The major features of the nephropathy were multiple episodes of metabolic acidosis, minimal proteinuria, pyuria but no bacteriuria, and polyuria and polydipsia early in the course of drug ingestion. Papillary necrosis was not a prominent clinical feature of this series. Discontinuation of drug ingestion by one patient was associated with recovery of a considerable degree of renal function. Preliminary experimental evidence obtained in the dog suggests that salicylate impaired the efficiency of the counter-current multiplier by decreasing sodium transport in the ascending limb of Henle, and decreased the permeability to water of the distal convoluted and collecting tubule; phenacetin had no such effect. (+info)
Downregulation of renal AQP2 water channel and NKCC2 in mice lacking the apical Na+-H+ exchanger NHE3.
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The apical Na+-H+ exchanger NHE3 plays an important role in fluid reabsorption in the proximal tubule. However, whether its deletion alters the salt and water transport in the distal nephron remains unknown. To answer these questions, wild-type (Nhe3+/+) and NHE3 null mice (Nhe3-/-) were placed in metabolic cages and their water balance and urine osmolality were examined. Nhe3-/- mice demonstrated a significant polydipsia (P < 0.03) and polyuria (P < 0.04), with a lower urine osmolality (P < 0.003) as compared to Nhe3+/+ mice. Northern hybridization and immunoblotting studies indicated that the mRNA expression and protein abundance of the collecting duct (CD) water channel AQP2 decreased by 52 % (P < 0.0003) and 73 % (P < 0.003) in the cortex, and by 53 % and 54 % (P < 0.002) in the inner medulla (IM) of Nhe3-/- vs. Nhe3+/+ mice. The expression of AQP2 in the outer medulla (OM) remained unchanged. Further, the mRNA expression and protein abundance of the medullary thick ascending limb (mTAL) apical Na+-K+-2Cl- cotransporter (NKCC2) decreased by 52 % (P < 0.02) and 44 % (P < 0.01), respectively, in the OM of Nhe3-/- vs. Nhe3+/+ mice. The circulating plasma levels of vasopressin as well as the mRNA expression of vasopressin prohormone were significantly increased in Nhe3-/- vs. Nhe3+/+ mice (P < 0.05). Studies in mice treated with acetazolamide indicated that increased bicarbonate and fluid delivery to distal nephron did not alter the expression of NKCC2 in mTAL and decreased AQP2 protein only in OM but not in the cortex or IM. In conclusion, mice lacking the apical NHE3 have impairment in their water balance and urine osmolality, which correlates with the downregulation of AQP2 expression. These defects occur despite increased circulating levels of vasopressin. We propose that an ADH-independent mechanism is responsible for the downregulation of AQP2 and the resulting polyuria in NHE3 null mice. (+info)
Reduced expression of renal Na+ transporters in rats with PTH-induced hypercalcemia.
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The purpose of this study was to evaluate whether the natriuresis and polyuria seen in parathyroid hormone (PTH)-induced hypercalcemia are associated with dysregulation of renal Na transporters. Rats were infused with three different doses of human PTH [PTH (1-34); 7.5, 10, and 15 microg.kg(-1).day(-1) s.c.] or vehicle for 48 h using osmotic minipumps. The rats treated with PTH developed significant hypercalcemia (plasma total calcium levels: 2.71 +/- 0.03, 2.77 +/- 0.02, and 3.42 +/- 0.06 mmol/l, respectively, P < 0.05 compared with corresponding controls). The rats with severe hypercalcemia induced by high-dose PTH developed a decreased glomerular filtration rate (GFR), increased urine output, reduced urinary osmolality, increased urinary Na excretion, and fractional excretion of Na. This was associated with downregulation (calculated as a fraction of control levels) of whole kidney expression of type 2 Na-P(i) cotransporter (NaPi-2; 16 +/- 6%), type 3 Na/H exchanger (NHE3; 42 +/- 7%), Na-K-ATPase (55 +/- 2%), and bumetanide-sensitive Na-K-2Cl cotransporter (BSC-1; 25 +/- 4%). In contrast, an upregulation of the Ca(2+)-sensing receptor (CaR) was observed. Rats treated with moderate-dose PTH exhibited unchanged GFR but decreased urinary concentration. The whole kidney expression of NHE3 (52 +/- 8%) and NaPi-2 (26 +/- 5%) was persistently decreased, whereas BSC-1 and Na-K-ATPase protein levels were not altered. CaR expression was also increased. Moreover, rats treated with low-dose PTH showed very mild hypercalcemia but unchanged GFR, normal urinary concentration, and unchanged expression of Na transporters and CaR. In conclusion, the reduced expression of major renal Na transporters is likely to play a role in the increased urinary Na excretion and decreased urinary concentration in rats with PTH-induced hypercalcemia. Moreover, the increase in the CaR in the thick ascending limb (TAL) may indicate a potential role of the CaR in inhibiting Na transport in the TAL. (+info)