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PubMed1986

Xylazine-ketamine-induced anesthesia in rats and its antagonism by yohimbine.

A combination of xylazine and ketamine was used to anesthetize 60 male rats, and then yohimbine was given to evaluate its reversing effect on xylazine-ketamine-induced anesthesia. In experiment A, xylazine (21 mg/kg of body weight) and ketamine (45 mg/kg) were admixed and administered IM to 12 Sprague-Dawley rats. Anesthesia lasted approximately 70 minutes. The xylazine-ketamine combination also induced polyuria, bradycardia, and bradypnea. When yohimbine (2.1 mg/kg) was given intraperitoneally 20 minutes after the xylazine-ketamine injection, the rats regained consciousness and righting reflexes within approximately 10 minutes. Yohimbine also reversed the bradycardia and bradypnea and appeared to reduce the polyuria induced by the xylazine-ketamine combination. In experiment B, xylazine (15.4 mg/kg) and ketamine (33 mg/kg) were admixed and given IM to 48 Holtzman rats. The combination induced surgical anesthesia for at least 30 minutes, during which a surgical procedure involving grafting a section of the sciatic nerve into the hypothalamus was performed. In rats in which yohimbine (1 mg/kg) was given intraperitoneally 45 to 60 minutes after xylazine-ketamine administration (before natural recovery from the anesthesia), the righting reflex was apparent in less than 10 minutes.

Anesthesia, General↗
PubMed1987

Renal injury induced by long-term administration of cyclosporin A to rats.

Chronic administration of cyclosporin A (CyA) to animals and humans results in renal damage characterized by tubulointerstitial lesions and renal insufficiency. This nephrotoxicity limits the use of CyA in the management of graft rejection. Despite recent investigations in this area, relatively few studies correlate structural and functional abnormalities in animals undergoing long-term CyA treatment. The authors therefore treated 30 rats with CyA at the dose of 40 mg/kg/48 hr for up to 5 months. An additional group of 30 rats was given the vehicle alone and was considered as a control group. Renal morphology and function were studied. For evaluation of the effect of drug withdrawal, a third group of 25 animals received CyA for 3 months and was followed for another 2 additional months after drug withdrawal. The results show that the chronic administration of CyA to rats induced complex renal morphologic changes, associated with renal insufficiency, polyuria, and enhanced sodium excretion. Withdrawal of the drug resulted in almost complete normalization of morphologic and functional parameters. The early morphologic expression of CyA nephrotoxicity was isometric vacuolization and loss of brush border involving the proximal tubular cells, followed by a peculiar lesion in distal tubular cells due to glycogen accumulation. Glomerular and interstitial damage was mild and appeared only after 3 months of CyA administration. No vascular abnormalities were found in rats treated with CyA for 5 months. A CyA-induced decrease in the glomerular filtration rate (GFR) correlates with brush border loss but not with isometric vacuolization. The distal tubular glycogen accumulation was associated with the development of polyuria and enhanced sodium excretion. Given the high blood sugar level and severe glycosuria in animals treated chronically with CyA, it is also concluded that CyA possesses a diabetogenic effect which is likely to be responsible for glycogen accumulation at the tubular level.

Animals↗
PubMed1986

Nephrogenic diabetes insipidus presenting with infantile hypotonia. A report of 2 cases.

Nephrogenic diabetes insipidus usually presents with polyuria, polydipsia, fever, vomiting, dehydration and failure to thrive. However, in infancy polyuria may be absent because of dehydration and reduced glomerular filtration rate. In 2 cases the main presenting feature was hypotonia, with marked head lag. Family studies confirmed the X-linked mode of inheritance of the disease; in case 1 the disease appeared to have arisen as a new mutation in the mother, and in case 2 the carrier status was traced back to the great-grandmother. Pitfalls in the diagnosis and detection of the carriers are discussed. Treatment with thiazide diuretics and prostaglandin synthesis inhibitors is effective in reducing urine volumes and polydipsia. The early detection of the disease and adequate management may prevent such complications as megacystis, mega-ureter and hydronephrosis, with resulting renal failure. Mental and physical retardation may also be avoided.

Anorexia↗
PubMed1985

Detection of latent bacteriuria in patients with chronic pyelonephritis.

Diagnostic possibilities of selective examination of renal urine particularly collected under medicamentous polyuria conditioned by the administration of Lazix were studied in latent bacteriuria. By means of separate collection of renal urine against the background of polyuria it was possible additionally to detect bacteriuria in 1/3 of the patients, to record increase in the intensity of the index in almost half of the patients with renal bacteriuria and, in 1/4 of them to detect, in renal urine, the aetiological agent absent from bladder urine. The latter circumstance not only has a diagnostic significance but also plays a certain role in the selection of medicamentous therapy in chronic pyelonephritis. In addition to traditional bacteriological methods, filtration through membrane filters was used to isolate and identify microflora in the urine. By means of this method it is possible to detect extremely low bacteriuria which cannot be established by any other method.

Bacteria↗
PubMed1985

The effects of piretanide capsules on blood pressure during ergometric and isometric work loads in patients with mild to moderate essential hypertension.

A single-blind study was carried out in 22 out-patients with mild to moderate hypertension to investigate the effects of piretanide capsules on systolic and diastolic blood pressure during standardized ergometric and isometric exercise. After a 4-week run-in period on placebo, patients received 1 capsule (6 mg) once daily for 6 weeks. If diastolic pressure was normalized (less than 95 mmHg), this dosage was continued for a further 6 weeks; patients whose blood pressure remained high after the initial 6 weeks received 1 capsule twice daily for a further 6 weeks. Significant reductions in blood pressure (9.2% for systolic, 14.6% for diastolic) were measured after 12-weeks' treatment during maximum ergometric work load exercise; during isometric exercise the reductions were 8.1% and 12.4%, respectively. The pulse-pressure product (a parameter indicating myocardial oxygen consumption), calculated for maximum ergometric exercise, was also significantly reduced by 8.8% after 12-weeks' active drug treatment. Serum levels of potassium, creatinine, urea, uric acid and cholesterol showed no clinically relevant changes during treatment. Side-effects definitely or probably associated with piretanide were observed in 13 patients. These, however, were generally mild and did not lead to interruption of piretanide treatment. Transient polyuria was reported by 5 patients during the first 2 weeks of active drug treatment; only 3 patients reported mild polyuria after 12 weeks of active drug treatment. The beneficial effect of piretanide especially on systolic blood pressure during exercise was in marked contrast effect of piretanide especially on systolic blood pressure during exercise was in marked contrast to the lack of such an effect reported during treatment with thiazide and other thiazide-like diuretics.

Adult↗
PubMed1974

Familial juvenile nephronophthisis. Experience with eleven cases.

Familial juvenile nephronophthisis (FJN) has an incidence in British Columbia of 1 per 50000 live births which gives a heterozygote frequency of 1 per 115. The authors report six families with a total of 11 cases. Multiple affected sibs are described in three families and in no instance was the condition present in more than one generation. The inheritance pattern is consistant with an autosomal recessive trait. The characteristic features are polyuria and azotemia though the presenting features may be either anemia or growth retardation with polyuria being elicited in the functional inquiry. There is a very hypotonic urine and absence of urinary sediment. Decreasing renal function at a variable rate is the fate of these patients, three of whom have had cadaver transplants.

Adolescent↗
PubMed1979

[Polycystic kidneys in adults. A clinical study of 106 cases (author's transl)].

A series of 106 cases of polycystic kidneys in adults is presented. The main clinical, exploratory and therapeutic data are analyzed. The average age of the patients at the time of the first clinical manifestation was 35 years; average age at the time of diagnosis was 43 years. The most common forms of presentation included renal colics, blood hypertension, noncolic lumbar pain, macroscopic hematuria, and polydipsia-polyuria. The most frequent symptoms were: abdominal pain of any type (73 patients), polydipsia-polyuria (66 patients), blood hypertension (61 patients), macroscopic hematuria (47 cases), episodes of urinary infection (41 cases), and passing of calculi (22 cases). Seventy-eight subjects had arterial high blood pressure; it was easily controlled in all except 14 cases. Proteinuria was slight in all except two cases. Values for hematocrit and hemoglobin remained high in relation to the degree of renal insufficiency. The mean value of hematocrit in patients with creatinine clearance below 10 ml/min was 30 percent. Renal function decreased gradually, from normal to a clearance of less than 10 ml/min over a period of 12 years on the average. Diagnosis was based mainly on abdominal physical examination and intravenous urography; 89 patients had palpable abdominal masses. Urography revealed typical images of polycystic kidney in every case. The following associated conditions were also discovered: liver cysts (17 cases among 57 liver scanning; bilateral ovarian cysts in one case; Cacci-Ricci's disease in one case; and cerebral arterial aneurysms in another patient. Treatment was conservative with the aim to control arterial blood pressure and urinary infection. Twenty-nine patients required saline replacement; peritoneal dialysis was practiced in two cases and permanent hemodialysis was prescribed for 15 individuals.

Adolescent↗
PubMed1979

[Recent developments in lithium treatment: is the kidney affection dangerous? (author's transl)].

In our hospital, we are studying the renal function of more than 200 patients under lithium treatment. The glomerular function seems to be affected to a small extent, even by long-term lithium administration, and there have been no instances of progressive deterioration of renal function with azotemia. Most of the patients have impaired water reabsorption with polyuria and polydipsia. This is frequently combined with lowered concentrating ability. Polyuria and lowered concentrating ability are not in themselves life-threatening. However, development of dehydration may lead to lithium poisoning, and patients under lithium treatment should be advised to drink extra fluid under circumstances when the fluid balance may become negative. Further studies are required for definitive recommendations concerning extra monitoring of kidney function and lowering of lithium doses.

Bipolar Disorder↗
PubMed1983

Nephrotoxicity of 1-(2-chloroethyl)-3-(trans-4-methylcyclohexyl)-1-nitrosourea (MeCCNU) in the Fischer 344 rat.

A single s.c. injection of 1-(2-chloroethyl)-3-(trans-4-methylcyclohexyl)-1-nitrosourea (MeCCNU; 20-140 mg/kg) resulted in rapid decreases in renal function as well as leading to a chronic progressive nephropathy in male Fischer 344 rats. Disturbances in renal function were proportional to the dose of MeCCNU administered and included impaired tubular transport of p-aminohippuric acid, a decrease in urine concentrating ability, an increase in urine pH, polyuria, proteinuria and enzymuria. The tubular accumulation of p-aminohippuric acid by kidney slices was decreased as early as 1 hr after MeCCNU administration (100 mg/kg), was maximal within 12 hr and remained depressed for at least 28 days after a single injection of either 40 or 80 mg/kg. Changes in other measures of renal function (increased lactate dehydrogenase excretion, alkalinuria and decreased urine concentrating ability) were delayed from 1 to 6 days after MeCCNU administration and in some cases progressed in severity throughout the 28-day duration of the experiment. The delay between the first evidence of renal damage (decreased p-aminohippuric acid uptake) and the subsequent appearance of enzymuria, proteinuria, polyuria and alkalinuria appears to correspond to a similar delay between the initial insult and the eventual development of cellular necrosis and other histopathological changes. These results demonstrate that MeCCNU is a nephrotoxicant in rats and indicate that even a single acute dose may lead to chronic and irreversible effects on the kidney. The in vivo toxicity model defined herein appears to be an appropriate one for further study of the mechanism of nephrotoxicity of MeCCNU.

Animals↗
PubMed1984

Diabetes insipidus: occurrence after minor head trauma.

Post-traumatic diabetes insipidus is a rare entity, usually associated with severe head trauma, often with skull fracture and cranial nerve dysfunction. A 24-year-old male presented to a medical clinic 2 weeks after a minor head injury with presenting symptoms of polyuria with nocturia and intense polydipsia. A diagnosis of post-traumatic diabetes insipidus was made. Although other causes of polyuria syndromes must be ruled out, plotting urine versus plasma osmolalities can provide rapid preliminary diagnostic help when considering diabetes insipidus. First-line treatment should include a trial of chlorpropamide and hydrochlorothiazide. Caution should be exercised in not overlooking associated anterior pituitary damage, which may develop several years post-trauma.

Adult↗
PubMed1984

Effects of long-term lithium administration on renal structure and function in rats. A distinctive tubular lesion.

Because lithium salts are widely used for long-term therapy of affective disorders and have been recently implicated as a cause of tubulointerstitial renal disease, we have undertaken experiments designed to establish the site of the early and late pathologic lesions and to determine their correlation with the lithium-induced concentrating defect. Male Wistar rats given a semisynthetic diet that contained lithium carbonate, 90 mEq/kg dry weight, developed serum lithium levels in the human therapeutic range; pair-fed controls received sodium carbonate. Within 3 weeks, treated rats developed marked polyuria, with elevation of free water clearance and vasopressin-resistant diabetes insipidus. Early morphologic changes were confined to the cortical collecting tubules and, possibly, contiguous portions of distal tubules. The tubules were dilated and irregularly lined with cells that had bulging or thinned basophilic cytoplasm, enlarged nuclei, sometimes basal vacuolization, and a few mitoses. These changes were evident at 3 weeks and progressed through the end of the observation period at 18 weeks. The proliferative component of the lesion was demonstrated by the finding of a significant and specific increase in 3H-thymidine uptake by nuclei of collecting/distal tubules of lithium-treated rats. The lesion, but not the increased thymidine uptake, extended into the medullary collecting ducts at 9 and 18 weeks. Although occasional intratubular mononuclear cells were seen at 9 and 18 weeks, no interstitial inflammation or fibrosis was seen. These tubular epithelial lesions were not seen in the kidneys of Brattleboro rats or glucose-treated Wistar rats despite comparable polyuria. We suggest that this early, persistent, and reproducible lesion, characterized by reactive and proliferating tubular cells in the cortical collecting tubules, predisposes the kidney to injury from otherwise mild or insignificant insults and may explain the sporadic occurrence of serious tubulointerstitial disease in patients on long-term lithium therapy.

Animals↗
PubMed1978

Renal biosynthesis of prostaglandin E2 and F2alpha: dependence on extracellular potassium.

Since recent investigations have shown elevated urinary PGE2 and polyuria in hypokalemic animals which were reversed by PG synthesis inhibition with indomethacin, studies were undertaken to examine the effects of extracellular [K+] on renomedullary PG production in vitro. Slices of rabbit and human renal papilla were incubated in Krebs-Ringer HCO3- buffer, 95% O2-5% CO2, glucose 10 mM, HSA 4 gm/100 ml, for 30 min at 38 degrees C, with and without 1-14C-AA (10 micrometer). Measurments were made of total endogenous iPGE2 and iPGF2alpha production and radioactive AA leads to PGE2. In rabbit renal medulla values for iPGE2 (nmol/gm/30 min) were 252 +/- 20 at [K+] 0; 182 +/- 17 at [K+] 2.5 mEq/L; 163 +/- 18 at [K+] 5.5; and 129 +/- 17 [K+] 9.0 (p less than 0.005). iPGF2alpha was unaltered by changes in media potassium concentrations (6.8 +/- 0.9 nmol/gm/30 min at [K+] 0 and 6.2 +/- 0.8 at [K+] 9.0 MEq/L). In the human renal medulla iPGE2 was 9.5 +/- 1.6 nmol/gm/30 min at [K+] 0; 5.0 +/- 0.7 at [K+] 2.5 mEq/L; 5.3 +/- 0.3 at [K+] 5.5; and 4.6 +/- 1.0 at [K+] 9.0 (p less than 0.05). AA leads to PGE2 (nmol/gm/30 min) was 3.21 +/- 0.92 at [K+] 0; 2.47 +/- 0.57 at [K+] 2.5 mEq/L; 1.30 +/- 0.30 at [K+] 5.5; and 0.76 +/- 0.4 at [K+] 9.0 in rabbit medulla (P less than 0.005). It is postulated that direct stimulation of papillary PGE2 biosynthesis by low extracellular [K+] impairing the cAMP-generating response to vasopressin could represent the initial event in the pathogenesis of vasopressin-resistant polyuria.

Animals↗
PubMed1981

[Diabetes insipidus induced by post-resuscitation hypoxia].

A 13-year-old girl was admitted with meningeal signs. A lumbar puncture was followed shortly by cardiorespiratory arrest. In spite of intensive resuscitation she remained comatose and severe polyuria diagnosed as diabetes insipidus appeared. The differential diagnosis of dehydration and polyuria in patients after cardiorespiratory arrest and resuscitation should include hypothalamic injury causing diabetes insipidus.

Adolescent↗
PubMed1981

Fine structural study of the posterior pituitary after destruction of the hypophysial stalk in the rat.

Electrolytic destruction of the pituitary stalk in rats markedly affected their water metabolism and induced ultrastructural changes in the posterior pituitary. The urinary output increased for 1-2 days after surgery. Subsequently polyuria and polydipsia temporarily decreased and vasopressin excretion with the urine increased. This oliguric interphase was followed by permanent polyuria and polydipsia. No ultrastructural changes were apparent for a few hours after surgery, but 3-5 days later the number of electron-dense granules of the axons decreased and conglomerated in the form of multilamellar bodies. Phagocytic and excretory phenomena were observed in the cytoplasm of endothelial cells and pericytes. The nuclei of pituicytes became loosened, and 5 days following surgery the mitochondria showed swelling and ruptures. The Golgi apparatus and the RER were prominent at 14 days, while degenerative lipid droplets accumulated in the cytoplasm. The fine structural findings, in agreement with the functional observations, support the assumption that the oliguric interphase is due to excessive discharge of vasopressin from the degenerating neural lobe of the pituitary.

Animals↗
PubMed1995

[Nonobstructive urinary tract dilatation due to diabetes insipidus in a patient with craniopharyngioma].

A 46-year-old man who had a history of hypogonadism, bilateral hydronephrosis and huge residual urine volume during the past ten years was admitted complaining of fever and flank pain. Polyuria which was more than 4 liters per day and inability of urine concentration suggested diabetes insipidus. Magnetic resonance imaging (MRI) demonstrated a tumor which was compatible with craniopharyngioma. Tumor resection and administration of desmopressin improved polyuria and urinary tract dilatation with marked reduction of residual urine volume from 400 ml to 20 ml.

Craniopharyngioma↗
PubMed1995

[A case of pulmonary eosinophilic granuloma and diabetes insipidus].

A 31-year-old man was admitted to our hospital because of a sudden onset of thirst, polyposia, and polyuria. Five years previously he had been admitted to our hospital because of a dry cough. On the first admission, the chest X-ray film had shown reticular shadows and bullous changes in both upper lung fields. Histological examination of a transbronchial lung biopsy specimen had revealed that the nodular lesion in the interstitium of the alveolar lesion consisted of an aggregate of many Langerhans cells with pale cytoplasm and partly convoluted nuclei. In addition, immunoperoxidase stain for S-100 protein had been strongly positive in numerous Langerhans cells in a bone biopsy specimen from a left mandibullar lesion, which is the same histological appearance as the lung lesion. A diagnosis of pulmonary eosinophilic granuloma had been made. The course after discharge was not progressive without treatment for 5 years, but the patient suddenly began to have thirst, polyposia, and polyuria. Dehydration, vasopressin tests, and the findings of MRI indicated diabetes insipidus due to a pathological change in the pituitary gland. Although diabetes insipidus is known to be a common complication of pulmonary eosinophilic granuloma, only 9 cases have been reported in Japan.

Adult↗
PubMed1993

Lithium nephrotoxicity.

After nearly two decades of concern and controversy surrounding the long-term effects of lithium on the kidney, the fact that lithium is capable of causing a major disturbance in water balance, manifest as polyuria and secondary polydipsia, remains undisputed. A decreased urinary concentrating ability (nephrogenic diabetes insipidus) with a disturbed responsiveness of the distal nephron to the action of ADH (vasopressin) is demonstrable, and the symptoms are largely reversible on cessation of lithium or reduction of the dose. An acute histological lesion of the distal nephron, corresponding to the site of lithium inhibition of the action of ADH, and consisting of epithelial cellular swelling and glycogen deposition, also appears to be readily reversible. Of greater concern is the development of a progressive impairment of urinary concentrating ability in patients on long-term maintenance therapy--especially those with a history of acute lithium toxicity and those additionally treated with neuroleptics. This functional lesion is not always reversible, and the underlying renal histology is a chronic focal interstitial nephropathy. Interestingly, some psychiatric patients never exposed to lithium have demonstrated similar renal histology. There is very little evidence that stable maintenance lithium therapy, without episodes of acute intoxication, is associated with a reduction of glomerular filtration rate. Episodes of acute lithium intoxication are largely predictable, and therefore avoidable, provided appropriate precautions are taken. Patients with polyuria and impaired urinary concentrating ability are at increased risk of acute lithium toxicity because of excessive renal losses of fluid, and these symptoms should be treated in the first instance with dosage reduction.(ABSTRACT TRUNCATED AT 250 WORDS)

Glomerular Filtration Rate↗
PubMed1996

Nutritional management of the child with mild to moderate chronic renal failure.

1. The best way to prevent early growth failure in children with renal disease is by the use of specified nutrition and appropriate buffer, activated vitamin D, and calcium-containing phosphate binders as needed. With prenatal diagnosis of anatomically abnormal kidneys available, this type of early intervention may be much more feasible in the 1990s. 2. Supplemental sodium and water in children with polyuria and intravascular volume depletion may prevent growth failure. Cow milk is detrimental in this group of individuals because of high solute and protein load, often causing intravascular volume depletion, hyperphosphatemia, and acidosis. 3. Children with acquired glomerular disease may need sodium restriction and, if treated with steroids, a diet low in saturated fat. 4. Children with nephrotic syndrome and severe edema should be evaluated for malabsorption and subsequent malnutrition. Protein intake should be supplemented only at the RDA and to replace ongoing losses. Long-term sodium restriction is appropriate. Hyperlipidemia should be monitored: if nephrosis is chronic, a low saturated fat diet should be instituted. Angiotensin-converting enzyme inhibitors can decrease urinary protein loss and may ameliorate hyperlipidemia. Children resistant to therapy can have very high morbidity. 5. Children with <50 % of normal creatinine clearance should have PTH measured and activated vitamin D therapy should be started if PTH is elevated more than two to three times normal. Thereafter careful monitoring of calcium, phosphorus, and PTH is crucial to prevent renal osteodystrophy, low turnover bone disease, and hypercalcemia with hypercalciuria and nephrocalcinosis. 6. Children with tubular defects with severe polyuria also may benefit from low-solute, high-volume feedings. 7. All physicians caring for children with renal disease should have pediatric nephrology consultation available. Prevention of growth failure is much more cost effective than pharmacologic therapy. Before initiating growth hormone treatment for growth retardation, assiduous treatment of co-existing renal osteodystrophy and provision of optimal nutritional intake should be accomplished.

Calcium↗