Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Azotemia”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 541 records · Page 30Linked to original sources
PubMed1987

Renal effects of angiotensin-converting enzyme inhibition in cardiac failure.

Compensatory mechanisms such as systemic vasoconstriction and sodium retention are activated to various degrees in patients with congestive heart failure (CHF). The renin-angiotensin system (RAS) mediates many of these compensatory responses. Increased angiotensin can result in net vasoconstriction and increase afterload. In addition, it contributes to the avid sodium retention that occurs in patients with CHF. The RAS promotes sodium retention by enhancing proximal tubular reabsorption of sodium and water through changes in intrarenal hemodynamics. In addition, the direct renal tubular influence of angiotensin II and aldosterone contribute to sodium retention. In experimental heart failure in the rat, angiotensin activation leads to reduction in effective plasma flow whereas the glomerular filtration rate was unchanged. In clinical CHF, activation of the RAS may also contribute to azotemia in patients with CHF. Significant correlations between serum creatinine levels and plasma renin activity have been observed. Furthermore, renal plasma flow and the glomerular filtration rate frequently improve after therapy with converting-enzyme inhibitors (CEIs). Occasionally, however, CEIs may produce an excessive fall in systemic BP and, hence, renal perfusion pressure, which may overcome autoregulatory mechanisms and contribute to a deterioration in renal function. CEIs enhance the effectiveness of furosemide in promoting natriuresis and correction of hyponatremia. Diuretic-induced hypokalemia can also be corrected by angiotensin-converting enzyme (ACE) inhibitors due to blockade of aldosterone production. On the basis of these results, we recommend titration of the ACE inhibitors' dose to minimize hypotension and the concurrent use of furosemide in patients with CHF receiving ACE inhibitors, especially for those in whom azotemia, hyponatremia, and hypokalemia complicate the course.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1988

Metabolic and renal effects of interleukin-2 immunotherapy for metastatic cancer.

The systemic administration of recombinant interleukin-2 (IL-2) either alone or in combination with lymphokine activated killer cells is a new approach to the immunotherapy of metastatic cancer in man. Renal toxicity is often a dose-limiting side effect of IL-2 administration. This prospective study of 17 consecutive patients receiving parenteral high dose IL-2 documents a reversible syndrome of hypotension, oliguria, fluid retention, azotemia and very low urinary excretion of sodium (median FeNa of 0.04%). The median nadir urinary uric acid to urinary creatinine ratio during IL-2 therapy was 0.2. This IL-2 regimen induces a reversible renal hypoperfusion syndrome (pre-renal azotemia) without evidence of acute uric acid nephropathy. Hypophosphatemia [median serum phosphorus of 1.9 mg/dl (0.61 mmol/l)] prompted further study of tubular function. Urinary excretions of phosphorus, calcium and magnesium were very low. Arterial blood gases revealed hyperventilation without alkalemia. The hypophosphatemia probably reflects increased utilization of inorganic phosphorus by rapidly proliferating lymphoid cells.

Acute Kidney Injury↗
PubMed1977

[Extramembranous glomerulitis. Apropos of 92 cases].

92 cases of extramembranous glomerulitis (EMG) documented by histology and immunofluorescence have been studied. At the time of renal biopsy the clinical and biologic picture was as follows: no proteinuria in 2%, isolated proteinuria in 18%, nephrotic syndrome without hypertension or azotemia in 41%, and hypertension and/or azotemia associated with proteinuria or nephrotic syndrome in 39%. A possible cause of the EMG was found in 27 cases: it was drug-induced or toxic in 10 instances, paraneoplastic in 7, lupus in 5 and parasitic (loasis) in 5.65 cases are regarded as idiopathic. The evolution is known in 66 cases and varies with the etiology: it is usually benign in secondary forms except the paraneoplastic cases. In the idiopathic forms it results in hypertension or more or less severe chronic renal failure in 62% of cases. The prognosis cannot be established on the basis of the initial histology. No treatment has proved effective.

Adolescent↗
PubMed1988

Correction of bilateral ureteral defects in a foal.

Bilateral ureteral defects were diagnosed as the cause of depression and azotemia in an 8-day-old Thoroughbred filly. The azotemia resulted from accumulation of urine in the retroperitoneal area. A ventral midline laparotomy was performed, and defects found in both the left and right ureter were repaired. Uroperitoneum and abdominal distention, presumably from urine leakage at the left ureteral surgery site, were detected on the fourth postoperative day and necessitated abdominal drainage. Thirty-six hours later, the leakage stopped spontaneously, and the foal recovered normally. This report should help to differentiate ureteral defects in foals from the more common syndrome of ruptured bladder.

Animals↗
PubMed1988

Autosomal recessive polycystic kidney disease in a murine model. A gross and microscopic description.

The C57BL/6J-cpk genetic murine model of autosomal recessive polycystic kidney disease was examined to gain insight into the pathogenesis of renal cystic disease. Fetal through 3-week-old offspring of heterozygote matings were used to study growth parameters and morphology of this genetic form of cystic disease. The kidneys were examined by light and electron microscopy and nephron segments were microdissected. Two phases of cystic disease development were morphologically identified. The first phase in fetal and newborn affected pups was characterized by proximal tubule enlargement and a general increase in the tubular mitotic index. The proximal tubules showed cytologic abnormalities along with an increased necrotic cell index. The later phase, in one through 3-week-old cystic pups, was characterized by progressive enlargement of the kidneys due mainly to cystic change of the collecting ducts and by development of azotemia. Secondary to the azotemia was a stunted body growth. Significant tubular epithelial hyperplasia was not found by mitotic index during the second phase, but an increase in collecting duct cellularity was present. Histone H4 gene expression, which is tightly coupled to DNA synthesis and thus an index of cell proliferation, showed only a minimal increase in cystic kidneys at 1, 2, and 3 weeks of age. Therefore, the degree of cell proliferation necessary to allow the observed tubular enlargement appears to be minimal.

Animals↗
PubMed1986

The usefulness of micro- and macrochromatographic determinations of glycohemoglobin in diabetic patients with nephropathy.

Determination of glycohemoglobin in blood (HbA1) represents an established measure of glycemic control in diabetic patients. In patients with uremia, however, the determination can be subject to pitfalls which may limit its reliability. In order to evaluate the clinical usefulness of HbA1 determinations in diabetic patients with nephropathy, concentrations of HbA1 and its subfractions HbA1c and HbA1a+b were measured by micro- and macrocolumn chromatography in 58 diabetic and 80 non-diabetic patients with impaired renal function. Fifteen diabetic patients without nephropathy and 15 healthy subjects served as controls. The concentrations of HbA1 and its subfractions were significantly higher in non-diabetic patients with nephropathy than in healthy controls. A positive correlation was seen between HbA1 and plasma glucose concentrations in all subjects, and between HbA1 and serum urea and creatinine concentrations in the non-diabetic subjects. When measured repeatedly in the same patient there was a positive correlation between HbA1 and plasma glucose concentrations in diabetic patients with azotemia. There was no change in HbA1 concentrations measured immediately before and after hemo- or peritoneal dialysis. The increase of chromatographically determined HbA1 concentrations in azotemic patients is most likely due to the joint action of carbamylation of hemoglobin with urea derived cyanate and deterioration of glycemic control induced by azotemia. Despite these problems, chromatographically determined HbA1 is still a clinically useful measure of glycemic control in diabetic patients with nephropathy. This presumes repeated measurements in the same patient and the use of appropriate reference levels which consider the degree of renal impairment.

Adult↗
PubMed1987

Clinicopathologic, renal immunofluorescent, and light microscopic features of glomerulonephritis in the dog: 41 cases (1975-1985).

In a 10-year retrospective study, we evaluated the clinicopathologic features and renal immunofluorescence patterns of glomerulonephritis in 41 dogs. On the basis of results of histologic examinations, the dogs were segregated into 3 groups, including membranous (n = 12), mesangioproliferative (n = 15), or membranoproliferative glomerulonephritis (n = 14). No significant differences existed among groups in regard to age or duration of illness. Most dogs had been ill for one month or longer. The proportion of dogs with azotemia, anemia, and hyperphosphatemia were not different among the disease groups. Proportion of dogs with hypoalbuminemia and the severity of hypoalbuminemia were not different among groups. Highest urine protein losses and 24-hour urine protein/creatinine ratios developed in dogs with membranous glomerulonephritis. Although hypoalbuminemia and hypercholesterolemia were common (49%), the formation of edema or ascites was not (15%) and, therefore, few dogs had all of the classic features of the nephrotic syndrome. Few dogs suffered thromboembolic complications. Antinuclear antibody titers developed in 11 dogs, the highest titers developing in dogs with polyarthritis and systemic lupus erythematosis. Cellulose acetate electrophoresis detected alpha 2 and beta 1 globulin spikes in most dogs (87%). Results of renal immunofluorescence testing were positive in 36 dogs, using polyvalent antisera for immunoglobulins (Ig)G, IgA, IgM, and/or antisera for complement factor C3. When monovalent antisera for IgG, IgA, and IgM, and fibrinogen were used, immunofluorescence was not observed as often. The major fluorescent pattern was discrete multifocal segmental granular glomerular fluorescence, consistent with immune-complex deposition. Two dogs had linear glomerular staining patterns; however, antibodies directed against normal glomerular basement membrane were not found via elution studies. A high prevalence of glucocorticoid excess (treatment with glucocorticoids and spontaneous hyperadrenocorticism) (34%), chronic inflammatory skin disease (27%), neoplasia (17%), polyarthritis (12%), and systemic lupus erythematosis (7%) were observed as clinical problems concurrent with glomerulonephritis. In 5 dogs, treatment of glomerulonephritis with prednisolone (0.5 to 1.1 mg/kg) did not result in beneficial effects and in fact appeared to be detrimental, leading to azotemia and worsening proteinuria and physical condition in some of the dogs.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

Partial aortic ligation: a hypoperfusion model of ischemic acute renal failure and a comparison with renal artery occlusion.

Ischemic acute renal failure (ARF) in humans typically results from hypoperfusion, not total blood flow interruption. However, experimental studies of ischemic ARF have relied on total blood flow cessation models because no reliable hypoperfusion model has been described. Therefore, the goal of this study was to develop a hypoperfusion model of ischemic ARF and then to contrast it to a blood flow cessation model (renal artery occlusion). Rats were uninephrectomized, and then temporary (30 or 45 minute) partial aortic ligation (PAL) was created just above the left renal artery, yielding a renal perfusion pressure of 15 to 20 mm Hg and a renal blood flow of 0.1 to 0.2 ml/min. The severity of renal injury was assessed 24 hours later. Azotemia (30-minute PAL: BUN 47 +/- 5 mg/dl; 45-minute PAL: 118 +/- 11 mg/dl), depressed inulin clearances, and extensive pars recta proximal tubular necrosis resulted. Comparing 30 minutes of PAL with 30 minutes of renal artery occlusion revealed far less severe ischemic adenosine triphosphate depletion (P less than 0.001), less azotemia (P less than 0.05), less medullary vascular congestion (P less than 0.05), and less cast formation (P less than 0.05) with PAL. However, both models induced comparable degrees of tubular necrosis, oxidant tissue stress (as assessed by oxidized-reduced glutathione tissue assay), and post-ischemic adenosine triphosphate depletion. Both similarities and differences exist between hypoperfusion and blood flow cessation-induced experimental ARF. The difference indicate that blood flow cessation models may not closely simulate clinical ischemic renal injury.

Acute Kidney Injury↗
PubMed1987

Acute renal failure associated with administration of excessive amounts of tetracycline in a cow.

High doses of intravenously and intramuscularly administered oxytetracycline were believed to be responsible for acute renal failure in a dehydrated cow. Signs of renal disease included oliguria, perirenal edema, marked azotemia, moderate proteinuria, tubular casts in urinary sediment, and inability to concentrate urine. Concurrent intravenous administration of fluids and diuretics (mannitol and furosemide) resulted in reestablishment of normal urine production. Because of its nephrotoxic potential, oxytetracycline should be used cautiously and at recommended dosages in ruminants that have prerenal azotemia or otherwise reduced renal function.

Acute Kidney Injury↗
PubMed1986

Current concepts in clinical therapeutics: drug therapy in acute renal failure.

The etiology and classification, pathophysiology, diagnosis, clinical course, and drug therapy of acute renal failure (ARF) are reviewed. ARF, a rapid reduction in kidney function that results in decreased glomerular filtration rate and tubular function, is caused by many different factors and can cause multiple organ dysfunction. The major causes of ARF are classically divided into three broad categories: (1) prerenal, or hypoperfusion states, (2) intrarenal, or intrinsic renal parenchymal disease, and (3) post-renal, or urinary obstructive disorders. The underlying pathogenic abnormality is renal tubular cell damage in patients with prerenal azotemia; vascular and glomerular damage is often secondary to immunologic mechanisms. Interstitial nephritis, often drug-induced, results from an immunologically mediated inflammatory renal response. Obstructive nephropathy results from partial or complete blockade of urine flow. Diagnosis relies heavily on patient history and physical examination; laboratory data, renal imaging, and sometimes renal biopsy results can yield important clues. The clinical course of ARF consists of four phases: insult and onset, maintenance, diuresis, and recovery. Morbidity and mortality are high. Drug therapy is directed at preventing or reversing the renal lesion before ARF becomes established and supporting the patient to allow the body to correct the lesion once it occurs. Prevention of prerenal azotemia and intrarenal disease is directed at identifying patients at risk, minimizing nephrotoxicity, and maintaining adequate urine output. In patients with established renal failure, an appropriate intravascular volume and pressure must be re-established and underlying problems must be corrected. Fluid, electrolyte, and acid-base balance are critical, and other serious effects on the gastrointestinal and neurologic systems must be addressed. Even though morbidity and mortality remain unacceptably high in patients with acute renal failure, promising progress has been made during the last 20-30 years.

Acute Kidney Injury↗
PubMed1985

Fractional excretion of sodium. Exceptions to its diagnostic value.

Determining the cause of acutely deteriorating renal function is a common problem in clinical nephrology. The fractional excretion of filtered sodium (FENa) has been demonstrated to be a reliably discriminating test between prerenal azotemia and acute tubular necrosis. However, with increasing clinical use of the FENa, numerous reports of low FENa (less than 1%) have appeared. The clinical settings of these reports include oliguric and nonoliguric acute tubular necrosis, urinary tract obstruction, acute glomerulonephritis, hepatorenal syndrome, renal allograft rejection, sepsis, and drug-related alterations in renal hemodynamics. One particular urinary index cannot be expected to reliably discriminate between prerenal azotemia and acute renal failure in all cases. The utility of the FENa test in the differential diagnosis of acute renal failure must be interpreted in conjunction with the patient's clinical course and the use of additional urinary and serum tests.

Acute Kidney Injury↗
PubMed1977

[Modification of urea-N and creatinine levels using need-adapted amino acids during parenteral nutrition in patients under intensive care].

The present retrospective study concerns two sub-groups of patients having normal serum creatinine levels, adequate 24-hour urine volumes and no pathological changes in the serum or urine osmolarity. There are differences in the initial values of the serum urea nitrogen, the higher (with almost 60 mg%) being already in the azotemia range. Both sub-groups received 100 g of an amino acid mixture adapted to requirements in addition to comparable parenteral nutrition. This did not lead to non-physiological changes in urea nitrogen or any of the other parameters measured in either of the groups. The findings obtained allow the following conclusions to be drawn: Parenteral administration of a quantity of essential and non-essential amino acids adapted to requirements did not bring about a rise in urea nitrogen in either the patients with normal or raised urea nitrogen values. Hence there are not grounds for assuming that in the post-operative or post-traumatic phase the use of a mixture of essential amino acids is necessary to reduce potentially occurring azotemia.

Adult↗
PubMed1982

Effect of beta-receptor antagonists on HgCl2-induced acute renal failure in rats.

During the first 48 h of HgCl2-induced acute renal failure (ARF), a single intraperitoneal injection of 100-100 micrograms/kg of the beta-adrenergic blockers pindolol, propranolol and practolol caused a significant rise in urinary sodium excretion and a decrease in plasma renin activity (PRA), renal cortical renin activity (RRA) and urinary catecholamine excretion. A single intraperitoneal injection of 3 mg/kg HgCl2 resulted in ARF characterized by progressive azotemia, a transient increase in PRA, a progressive rise in RRA and urinary catecholamine excretion. After pretreatment with these beta blockers, PRA, RRA and urinary catecholamine excretion remained unchanged and azotemia was markedly reduced; urine flow rates did not fall, and were significantly higher than control flows till after 48 h. These results indicate that pretreatment with beta blockers decreases the severity of ARF, though they cannot prevent is; that increased activity of the sympathetic nervous system is involved in ARF and that increase in RRA may be an aggravating factor in the pathomechanism of the nephrotoxic model in ARF.

Acute Kidney Injury↗
PubMed1982

[Proliferating retinopathy in diabetes mellitus. Clinical and autopsy results].

UNLABELLED: Clinical and autoptic investigations of thirty patients suffering from diabetes mellitus and retinopathia proliferans result in these findings: Of the various manifestations of angiopathy only retinopathy (leading symptom), nephropathy, and arterial hypertension are present in all cases, all other forms receeding into the background numerically, though not in potency. 20 cases of nephropathy ended in uremia (cause of death), 10 cases in azotemia. In 14 out of 20 cases of uremia specific glomerulosclerosis (M. Kimmelstiel-Wilson) was stated autoptically, in the remaining 6 cases a different form of nephropathy was found (pyelonephritis, arteriosclerosis renum, chronic glomerulonephritis). In the 10 patients suffering from azotemia, direct causes of death were various general diseases, such as coronary sclerosis, encephalomalacia, pyogenic infections, and acute tuberculosis. CONCLUSION: Diabetes mellitus in connection with retinopathia proliferans turns out to be the most serious form of the general diabetic disease.

Adolescent↗
PubMedDate not supplied

[Effect of 24,25-dioxycholecalciferol on calcium-phosphorus metabolism and bone tissue in rats with experimental renal failure].

Experimental chronic renal failure (CRF) in rats gave rise to azotemia, hyperphosphatemia, reduction in the proportion of the diaphyses, decrease in them of calcium, phosphorus and hydroxyproline, and to the lowering of the calcium content in the epiphyses. Administration to the animals of 0.025 microgram of 1,25-dioxycholecalciferol (1,25(OH)2D3) a day did not make the indicators under consideration return to normal. At the same time 1,25(OH)2D3 enhanced the degree of hyperphosphatemia and demineralization of the epiphyses, provoked moderate hypercalcemia and dramatically enhanced calcinosis in the aorta and in the remainder of the kidney. Administration of 24,25-dioxycholecalciferol (24,25(OH)2D3) in a dose of 0.25 microgram made the majority of the indicators return to normal, increasing the proportion of the diaphyses and the content in them of calcium and phosphorus, reducing the blood phosphorus content and the degree of azotemia. Furthermore, 24,25(OH)2D3 raised the collagen content in the diaphyses and epiphyses. A higher dose of 24,25(OH)2D3 (1.25 microgram) did not appear more effective. In none the doses applied, 24,25(OH)2D3 produced hypercalcemia or calcinosis. Combination of 1,25(OH)2D3 in a dose of 0,025 microgram and 24,25(OH)2D3 in a dose of 1,25 microgram slightly reduced the hypercalcemic, hyperphosphatemic and calcinosis-inducing effects of 1,25(OH)2D3, completely prevented osteoporotic alterations in the diaphyses, but enhanced the demineralization in the epiphyses, which may point to the advisability of reducing the doses of these metabolites on combined use. The data obtained indicate that 24,25(OH)2D3 is a more effective and safer agent for correcting the disturbances of the phosphorus-calcium metabolism and osseous lesions in CRF than 1,25(OH)2D3.

24,25-Dihydroxyvitamin D 3↗
PubMed1984

[7 cases of congenital multicystic kidney with special reference to its embryogenesis].

We have experienced 7 cases of multicystic kidney. The latest two cases, etiologically of interest, are reported herein with special reference to its embryogenesis. Case 6: A 4-year-old girl was referred to our clinic for further evaluation of mild azotemia and nonvisualization of left kidney. Left kidney was strongly thought to be multicystic kidney from abdominal CT, whereas her contralateral kidney exhibited hydrocalycosis resembling infundibular stenosis with diminished calyceal numbers. Nephrectomy of her left kidney was performed and histological studies confirmed renal dysplasia (primitive duct, metaplastic cartilage, etc.). Case 7: A 7-year-old girl was referred to Hakodate Kyokai Hospital for the evaluation of azotemia and low stature. Her right kidney was not visualized on IVP and her left kidney exhibited hydronephrosis with diminished calyceal numbers. Her right kidney was diagnosed as multicystic kidney on CT-scan. Pyeloplasty of her left kidney was performed. Multicystic kidney is a rather rare congenital disease. Association of various anomalies in contralateral kidney has been emphasized as well as the notion that infundibulopelvic stenosis is a linked in the clinical spectrum extending from cystic dysplasia of the kidney to hydronephrosis. Our last two cases seem to be included in this category of obstruction theory. As shown by microdissection technique (Potter), however, severe ampullary inhibition early in fetal life is also an attractive hypothesis. Diminished calyceal number of contralateral kidneys seen in our recent two cases is compatible with possibility of ampullary damage. Recent experimental study also showed that renal dysplasia is not solely caused by simply mechanical obstruction to urinary drainage, even when the obstruction is imposed at an early stage of renal development.

Adolescent↗
PubMed1978

Characterization and treatment of acid-base and renal defects due to urethral obstruction in cats.

In 23 cats, urinary obstruction of 24 to 48 hours' duration caused marked azotemia, hyperphosphatemia, hyperkalemia, and metabolic acidosis. The metabolic acidosis was a consistent finding and was severe in all cats (venous pH, 7.11 +/- 0.09). Serum sodium and chloride were normal. Glycosuria was found in 17 (74%) of the cats. There was no clear difference in blood pH, serum chemical values, or electrolyte concentrations between cats obstructed 24 hours and those obstructed 48 hours or longer. At a mean of 8.4 hours after relief of obstruction, acid-base status was corrected to normal, using fluid replacement and sodium bicarbonate therapy. Blood urea nitrogen serum creatinine, and serum inorganic phosphorus improved significantly (P less than 0.01) at a mean of 19.5 hours after treatment. Variation in azotemia after fluid replacement suggested variable decreases in glomerular filtration rate after relief of obstruction. Hypokalemia occasionally developed after relief of obstruction during the postobstructive diuresis. It was concluded that fluid and electrolyte therapy must be regulated in response to the postobstructive diuresis, to ensure proper medical management.

Acid-Base Imbalance↗
PubMed1984

Primary renal disease in a dog.

A 7-month-old Lhasa Apso with a history of polydipsia and vomiting was depressed, thin and dehydrated. Serum chemistry assays revealed hyperphosphatemia and azotemia, and urinalysis revealed isosthenuria, suggesting azotemia of renal origin. Antemortem renal biopsy specimens contained several sclerotic glomeruli, a few embryonic renal tubules and interstitial fibrosis, indicating renal dysplasia.

Animals↗