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At least 991 records · Page 55Linked to original sources
PubMed1983

[Acute kidney failure following Cortinarius splendens (Fries) or "yellow clubbed foot" mushroom poisoning (so-called orellanus syndrome)].

Intoxications by cortinarii have only been recognized in recent years. Compared to other mushroom poisoning they are characterized by the long incubation time of up to ten days or more, and predominantly hepatorenal symptoms. In this paper the first two Swiss cases of intoxication with Cortinarius phlegmacium splendens are reported. The two patients ate two meals of this mushroom one week apart. Three days after the second meal the patients became acutely ill with severe lumbar pain, polyuria, polydipsia and constipation. Laboratory examinations revealed signs of hepato-renal toxicity with increase in serum creatinine, hyposthenuria and hyperbilirubinemia. Both patients recovered fully in the course of a further two weeks.

Acute Kidney Injury↗
PubMed1984

Nephropathic cystinosis in black children. Case reports.

Cystinosis is thought to be rare in Black patients. Two cases of nephropathic cystinosis in Blacks in early childhood are reported. One patient presented with classic features of Fanconi's syndrome with failure to thrive and rickets, while the other had polyuria, growth failure and rickets. This article highlights the need for the exclusion of cystinosis in any Black patient presenting with Fanconi's syndrome.

Acidosis, Renal Tubular↗
PubMed1984

[Sulpiride (stereoisomers, racemic) and dopamine: actions and interactions on renal circulation].

Interaction of sulpiride - both 1- and d- isomers as well as racemic- - with Dopamine (DA, subpressor dosage 0.1 microgram X kg -1 X min -1), on the renal hemodynamic, was studied in DOCA-pretreated men during hypotonic polyuria. P.A.H. and creatinine clearance and renal vascular resistances were determined. In the presence of d-Sulpiride, DA - induced renal vasodilation is carried out gradually and finally reaches similar levels as in the absence of d-Sulpiride. However no glomerular filtration rate increase is produced by DA. In the presence of 1-Sulpiride, DA vasodilating effect is suppressed. On the contrary a trend toward ischemia and a reduction in glomerular filtration rate becomes finally apparent. Stronger binding of 1- than d-Sulpiride with vascular DA receptors in suggested. When both isomers are simultaneously administered (at the nearly total dosage) much less inhibitory effect on DA vasodilator action is observed: it seems that each isomer decreases the affinity on the other isomer for vascular DA receptors.

Desoxycorticosterone↗
PubMed1984

[Sulpiride (stereoisomers, racemic) and dopamine: actions and interactions on tubular reabsorption].

In DOCA-pretreated men during hypotonic polyuria Dopamine (DA) infusion in a subpressor dosage (0.1 microgram X kg -1 X min -1) produces renal hyperemia, inhibition of isosmotic sodium reabsorption, increase in sodium distal load (s. d.l.) and finally inhibition of anisosmotic sodium reabsorption as a percentage of s.d.l. Such DA effects are variously modified by sulpiride isomers. Sodium distal load increase is still apparent in the presence of racemic, but not in the presence of either d- or l-Sulpiride isomers. However DA inhibition of anisosmotic sodium reabsorption % s.d.l. is unaffected by either or both Sulpiride isomers. If the DA tubular inhibition was dependent on specific DA receptors these receptors, unlike vascular DA receptors, would bind in a weaker way both d- and l-Sulpiride isomers.

Absorption↗
PubMedDate not supplied

[Dopamine as a regulator of natriuresis. Experimental bases and their implications].

Renal effects of dopamine (DA) infused i.v. in a subpressor dose (0.1 microgram. kg.-1 min-1) were investigated in healthy human subjects during steady hypotonic polyuria. In each experiment four clearance (cl.) periods of 15 min were performed; DA was administered during the second and the third cl. periods. The glomerular filtration rate and renal effective plasma flow were estimated as endogenous creatinine and PAH clearances. Moreover the following variables were evaluated: a) sodium total and sodium isosmotic reabsorption as a % of sodium filtered load (s.f.l.); b) sodium anisosmotic reabsorption as a % of sodium distal load (s.d.l.); c) total renal vascular resistance (RT), arteriolar afferent (RA) and efferent (RE) resistances. Three groups of experiments were performed: A) in hydro-saline retention by DOCA pretreatment (24 subjects); B) in hydro-saline depletion by natriuretic pretreatment (20 subjects); C) in hydro-saline depletion and beta-adrenergic blockade induced by natriuretic and propranolol pretreatments (9 subjects). In A experimental condition DA significantly increased renal plasma flow, glomerular filtration rate, urinary flow, urine sodium concentration and osmolarity; on the contrary DA significantly decreased RT, RA, sodium total and isosmotic reabsorption, % of s.f.l., and sodium anisosmotic reabsorption, % of s.d.l. In B condition no significant changes were observed during DA infusion in either haemodynamic parameters or urinary flow; on the other hand DA significantly blunted urinary osmolarity, urinary sodium concentration and sodium excretion rate suggesting an increased sodium anisosmotic reabsorption (% of s.d.l.). In C condition the vasodilating and hydrosaluretic effects of DA were restored. Our results suggest that DA activates, besides "dopaminic" vascular receptors, the presynaptic facilitory beta-adrenergic receptors in renal adrenergic pathways. Thus the renal action of DA depends on renal adrenergic activity.

Adult↗
PubMedDate not supplied

[Psychogenic polydipsia in a child].

At the age of 20 months a baby girl began with compulsive water drinking. The water intake reached 4,000 ml per day. The constant drinking of water created disorganization in the family life. At the age of 2 years and 9 months, the psychogenic polydipsia is confirmed, based in the patient's ability to concentrate her urine, which was demonstrated with 1-deamino-BD arginine vasopressin (DDAVP) and the water deprivation tests. Neither bacteriological, clinical, nor radiological evidences of urinary infection were found. The intravenous pyelogram revealed a unilateral and complete duplication of the collecting system. The abnormal urinary tract does not have a causal relationship with the polyuria. With progressive water deprivation, the polydispia stopped in two months. Psychogenic polydispia is rare in infants and children. The mistake and delay in diagnosis is frequency. The differential diagnosis with cranial diabetes insipidus and urological diseases may be difficult sometimes.

Child, Preschool↗
PubMed1980

[Partial defect in the secretion of antidiuretic hormone and disproportionate polydipsia (author's transl)].

A 20-year-old patient was evaluated because of polydipsia and polyuria; by means of the dehydration test a partial defect in the secretion of antidiuretic hormone (ADH) was demonstrated, since the urinary osmolality after the administration of exogenous vasopressin was superior by 25 percent to the maximum spontaneous urinary osmolality reached after a period of fluid restriction. Nevertheless, there was also a component of psychogenic polydipsia because the daily basal fluid intake was superior to 15 liters, and in view of the fact that the urinary osmolality could reach 600 mOsm/kg, the endocrine defect cannot totally be responsible for the enormous volume of fluid intake. This is the first case in the world literature in which the association between potomania and deficiency in the secretion of ADH is reported. Since ADH is one of the factors which regulate the behaviour of various animal species it is possible that its deficiency may be directly responsible for the psychic disorder which led to the potomania. It is also possible that an anatomical hypothalamic lesion, too small to be demonstrated, might have a simultaneous effect on the centers regulating thirst and the neurons producing vasopressin.

Adult↗
PubMed1980

Polyuric prerenal failure.

Prerenal failure is traditionally accompanied by oliguria and represents the normal renal adaptation to retain salt and water and correct the prerenal state. Nonoliguria occurring in the setting of acute renal failure usually represents acute tubular necrosis (ATN) since the kidney has lost its ability to extract salt and water. We report nine cases of patients with acute renal failure occurring in the setting of impaired systemic hemodynamic states and yet who were nonoliguric without strong evidence for ATN. The common defect in these subjects with "polyuric prerenal failure" was a blunted urinary concentrating ability. Polyuria and renal failure occurring despite evidence for impaired systemic hemodynamics may not necessarily be ATN, may still be prerenal, and should be recognizable and promptly reversible if treated appropriately.

Acute Kidney Injury↗
PubMed1995

[Simultaneous familial occurrence of distal renal tubular acidosis, polycystic kidney and nephrogenic diabetes insipidus].

In five members of three generations in a family studied in 1972, 3 nephrological disorders occurred concurrently: distal renal tubular acidosis (dRTA), polycystic kidney and nephrogenic diabetes insipidus (with the exception of a five-year-old child in whom polycystic kidney was not detectable--yet?). Chromosoma studies revealed an increased rate of the occurrence of variations. The youngest patient was reinvestigated in 1993; the other four affected members of the family were already not alive. 7 offsprings in two generations of the 3 healthy members of the third "patient generation" were healthy. The autosomal dominant way of inheritance characteristic to both dRTA and polycystic kidney disease was obvious in this family. On the other hand the same degree of the concentrating defect found both in the patients of the familial dRTA and in 11 control patients with non familial (acquired) dRTA suggested that the nephrogenic diabetes insipidus as an acquired disorder was associated with the two congenital abnormalities. The clinical picture of the combined disease was dominated by the symptoms of polydipsia and polyuria. The vasopressin resistance with a variation in the degree interindividually seemed to be responsible for the nephrogenic diabetes insipidus. Functional insufficiency of the loop of Henle was excluded on the basis of normal responses to a "loop diuretic".

Acidosis, Renal Tubular↗
PubMedDate not supplied

Synergistic effects of anti-gp330 and anti-dipeptidyl peptidase type IV antibodies in the induction of glomerular damage.

Passive Heymann nephritis (PHN) in the rat is induced by the administration of heterologous antibodies to renal tubular epithelium (RTE). The nephritogenic capacity of anti-RTE resides primarily in the antibody fraction directed against a 330-kD glycoprotein (gp330). However, monospecific anti-gp330 antibodies are less nephritogenic than anti-RTE antibodies. This discrepancy led us to study a possible synergizing role for different antibody specificities present within anti-RTE. The enzyme dipeptidyl peptidase type IV (DPP IV) is, like gp330, present in RTE as well as in the glomerulus. Anti-DPP IV antibodies have been shown to induce an acute, transient proteinuria. In this study, we investigated the nephritogenic effect of separate or simultaneous administration of heterologous anti-DPP IV and anti-gp330 antibodies. Injection of anti-DPP IV antibodies resulted in a short-lived glomerular binding, and in a dose-dependent polyuria, albuminuria or proteinuria. Binding of anti-gp330 antibodies was slower, but much more stable. Albuminuria could only be observed in the heterologous phase. Combined injection did not alter antibody-binding kinetics of either antibody nor the albuminuria induced by anti-gp330. However, in the presence of anti-gp330 antibodies, a lower dose of anti-DPP IV was capable to induce transient albuminuria as compared to anti-DPP IV alone. In conclusion, anti-DPP IV and anti-gp330 antibodies bind to different sites in the glomerulus with different kinetics. The presence of anti-gp330 deposits facilitated anti-DPP-IV-induced renal injury.

Albuminuria↗
PubMed1993

Diabetic ketoacidosis--a study of 33 episodes.

Twenty-six patients presenting with 33 episodes of Diabetic Ketoacidosis (DKA) and managed on a protocol oriented system were analysed. Diabetes mellitus was newly diagnosed at presentation in 18% of the 33 episodes. The presenting symptoms were polyuria and polydipsia (58%), nausea and vomiting (52%), change in sensorium (24%), hyperventilation (24%), and abdominal pain (18%). The main clinical findings at admission were dehydration (97%), acidotic respiration (67%), coma and confusion (61%), a clinically detectable source of sepsis (49%), fever (33%) and hypotension (9%). Blood sugar levels at admission ranged between 351 mg/dl and 1200 mg/dl (mean = 633 mg/dl). The mean serum potassium at diagnosis was 5.1 mmol/l and the mean calculated serum osmolality was 320 mOsm/kg. The mean serum osmolality was higher in those with disturbed conscious level. Infections, particularly those of the urogenital tract, were the main precipitating cause for the DKA. Only 12 of the 19 patients with sepsis had fever. Eight of the episodes were attributed to patients' non-compliance with insulin. Four patients died during the 33 hospitalisations, giving a mortality rate of 10%. Death occurred despite glucose control and stabilisation of the ketoacidotic state and was due to uncontrolled septicaemia. The mean duration of hospitalisation was 11 days. The ketoacidosis state was reversed after a mean duration of 9.5 hours, with an average soluble insulin requirement per patient of 52.4 units.

Adolescent↗
PubMedDate not supplied

Studies on renal function in healthy women with different degrees of induced potassium depletion. 1) Hormonal changes relevant to salt and water balance.

In healthy women we have studied the effects of potassium depletions of different degrees on the generation of some bioregulators of hydro-saline balance. The study has been performed on 20 women in normal potassium balance (N group) and 20 women submitted to potassium depletive treatment by dietary and pharmacological means. On the basis of different patterns of treatment we have obtained three groups i.e. KD1 (n = 8), KD2 (n = 6) and KD3 (n = 6) with potassium cumulative deficit of 160 +/- 43, 198 +/- 22 and 214 +/- 54 mmol, respectively. The renal function was assessed by the clearance method during induced hypotonic polyuria and subsequent moderate antidiuresis induced by low dose infusion of lysine-8-vasopressin. The urinary PGE2, 6-keto-PGF1 (6KPGF) and TxB2 were determined by the RIA method. Moreover, the basal PRA and urinary aldosterone were determined before the renal functional exploration. The data obtained in both KD2 and KD3 groups where renal hypokalemic dysfunctions occurred--indicate that hypokalemia stimulated renin secretion and inhibited the reactivity of renal prostanoid production to the polyuric stimulus. However, in the KD3 group--where the circulating levels of renin, and probably of angiotensin II were the highest--the hypokalemic depression of the synthesis of 6KPGF and TxB2 precursors was attenuated while the synthesis of PGE2 was still inhibited.

Adult↗
PubMed1993

Clinical aspects of renal involvement in Bardet-Biedl syndrome.

The Bardet-Biedl syndrome (BBS), which consists of polydactyly, obesity, mental retardation, pigmentary retinopathy and hypogonadism has been known since 1922, but due to the great similarity to the clinical manifestations of the Laurence-Moon syndrome (LMS) there is a considerable terminological confusion in the medical literature. An attempt is made at clarifying the problem. Four children from two families have been observed. There were inter- and intrafamilial variabilities of the expression and severity of the particular features, but retinopathy and structural and/or functional abnormalities were found in 100%. The combination of the two can serve as an easy clinical screening for diagnosis of the disease. Renal involvement is considered to be a cardinal feature of the syndrome. The most common and earliest symptoms are polydypso-polyuria and reduced concentrating ability, which may lead to some diagnostic difficulties, especially in infancy. Three children have end-stage renal disease and two of them are on maintenance haemodialysis, which they tolerate well.

Adolescent↗
PubMed1993

Primary parathyroid gland hyperplasia in dogs: six cases (1982-1991).

Persistent hypercalcemia attributable to parathyroid gland hyperplasia was identified in 6 dogs with primary hyperparathyroidism. Clinical signs included polydipsia (n = 4), polyuria (n = 4), and signs caused by cystic calculi (n = 3). Abnormal clinical pathologic findings included hypercalcemia (mean, 13.6 mg/dl; range, 12.6 to 14.7 mg/dl; n = 6), hypophosphatemia (mean, 2.2 mg/dl; range, 1.4 to 2.9 mg/dl; n = 6), high serum alkaline phosphatase activity (mean, 222 IU/L; range, 161 to 286 IU/L; n = 3), and isosthenuria (mean, 1.012; range, 1.006 to 1.017; n = 6). Serum parathyroid hormone concentration was within the reference range or high (mean, 23 pmol/L; range, 7 to 119 pmol/L; reference range, 1.5 to 13 pmol/L) in all dogs. At surgery, the number of large parathyroid glands was variable, being limited to 1 gland in 3 dogs, 2 glands in 2 dogs, and 4 glands in 1 dog. All visibly large parathyroid glands were surgically removed from each dog. Serum calcium concentration decreased into or below the reference range within 72 hours of surgery in all dogs, confirming the diagnosis of primary parathyroid disease. Multiple nodules of adenomatous hyperplasia were identified in each dog. All 6 dogs were treated with vitamin D and calcium carbonate following surgery. The dog from which all 4 parathyroid glands were removed has remained eucalcemic for more than 1 year with vitamin D supplementation. Vitamin D and calcium administration was discontinued within 4 to 12 weeks of surgery in the remaining 5 dogs. These dogs remained eucalcemic without vitamin D supplementation.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗
PubMedDate not supplied

Responses of the renal prostanoids to a short-term depletion of sodium or potassium in healthy women.

The short-term effects of extracellular fluid volume depletion on the generation of some bioregulators of the renal function have been studied in healthy women. Eight subjects (SD group) were submitted to a low NaCl dietary intake and natriuretic treatment. At the end of the treatment (6 days) a cumulative sodium deficit of 381 +/- 55 mmol (mean +/- SEM) and a body weight variation of -2.1 +/- 0.28 kg were estimated. The renal function was explored by clearance method during hypotonic polyuria induced by oral water load and subsequent antidiuresis induced by low-dose infusion of lysine-8-vasopressin. The basal values of plasma renin activity were determined just before the water load as well as the urinary aldosterone excretion of the foregoing 24 hours was. During the renal functional exploration the urinary concentrations of PGE2, 6-keto-PGF1 alpha (6KPGF) and TxB2 were determined by RIA method. We report also, as comparison terms, the results obtained either in potassium depletion (KD group, n = 12) or in normal sodium and potassium balance (N group, n = 20). 1) In the SD vs N group-besides the increase in renin and aldosterone secretion-the behaviour of urinary prostanoids is consistent with a stimulation of the renal synthesis of PGI2 and TxA2 as well as of PGE2, at least as a trend. 2) In the KD vs N group an increase in renin secretion occurred while the urinary aldosterone was not significantly decreased. The urinary prostanoid data suggest an inhibition of the renal synthesis of PGE2 and PGI2. All three urinary prostanoids were significantly lower in the KD as compared to the SD group. Thus, in salt depletion the renal prostanoid synthesis was enhanced while it was depressed in potassium depletion, despite the increased renin secretion.

Adult↗
PubMedDate not supplied

Interactions between acute effect of angiotensin converting enzyme inhibition and salt balance on the renal function and urinary prostanoids. Studies in healthy women.

The acute effects of angiotensin converting enzyme inhibition on the renal function and urinary prostanoids were studied. Healthy women were studied in both sodium depletion (n = 8) and normal balance of sodium and potassium (n = 6). Each woman underwent paired renal functional explorations (by the clearance method during hypotonic polyuria and subsequent antidiuresis) in the absence and in the presence of enalapril. In both experimental conditions enalapril failed to affect urinary prostanoid excretions. Only in the presence of hyperreninemia induced by salt depletion, enalapril was effective in inducing renal tubular effects only partly consistent with a depressed activity of angiotensin-aldosterone system. Specifically, in sodium depletion enalapril treatment promoted a decreasing trend in urinary salt excretion, dependent in turn on selective stimulation of the distal tubule NaCl transport. Furthermore, plasma potassium concentration was reduced despite the concomitant decrease in urinary potassium excretion.

Adult↗
PubMedDate not supplied

Side-effects of lithium.

An account of the side-effects of 30 patients treated with lithium at Athens University Department of Psychiatry during the last two years is presented. The most frequent side-effects were: tremor of bands, polydipsia, polyuria, increase in appetite, dryness of mouth, general muscular weakness and memory reduction. Most side-effects were infrequent, mild and in no case necessitated discontinuation of treatment.

Bipolar Disorder↗
PubMed1998

[Nephrogenic diabetes insipidus].

The syndrome of polyuria and polydipsia is practically identical in three very different disorders (central diabetes insipidus, nephrogenic diabetes insipidus, primary polydipsia). In congenital nephrogenic diabetes insipidus both the thirst mechanism and the production of the antidiuretic hormone are intact, but the hormone is ineffective in the kidney. The acquired form of the disease is caused most frequently by tubulointerstitial and urinary tract obstructive disorders as well as among the several drugs, lithium. In the differential-diagnosis the results of determinations related to the nomograms of normal interrelationships between osmolality and vasopressin in urine and plasma are used, besides the classical Carter-Robbins and indirect dehydration (Miller) tests. It has been postulated recently that in many cases the resistancy toward vasopressin is not absolute and these partially vasopressin sensitive patients can be treated successfully by thiazide, and potassium sparing compounds, antiprostaglandin pain killers (non-steroid antiinflammatory drugs) and first of all dDAVP as well as combinations of these preparations.

Diabetes Insipidus, Nephrogenic↗