PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Azotemia”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 19 recordsLinked to original sources
PubMed1982

Urinary indices for differentiation of prerenal azotemia and renal azotemia in horses.

The urine urea nitrogen/plasma urea nitrogen ratio (Uun/Pun), urine creatinine/plasma creatinine ratio (Ucr/Pcr), urine osmolality/plasma osmolality ratio (Uosm/Posm), and fractional excretion of filtered sodium (FENa) were evaluated in 16 horses with acute azotemia to ascertain the significance of each index in the differentiation of prerenal azotemia from renal azotemia. Renal azotemia was diagnosed when renal biopsy or postmortem histologic examination demonstrated evidence of organic renal disease or when azotemia was found in the presence of isosthenuria. The diagnosis of prerenal azotemia was based on the absence of renal histologic lesions or stabilization of blood urea nitrogen and serum creatinine soon after therapy. In 10 horses with renal azotemia, Uun/Pun was 2.1-14.3, Ucr/Pcr was 2.6-37.0, Uosm/Posm was 0.8-1.7, and FENa was 0.08-10.0. In 6 horses with prerenal azotemia, Uun/Pun was 15.2-43.7, Ucr/Pcr was 51.2-241.5, Uosm/Posm was 1.7-3.4, and FENa was 0.02-0.50. The values for each of these indices differed significantly between the 2 groups of horses (P less than 0.05). It was concluded that these indices were of value in the early classification of renal failure in the horse and that this information could be utilized in planning of therapy of acute azotemia in the horse.

Acute Kidney Injury↗
PubMed1990

Decreased fractional excretion of urate as an indicator of prerenal azotemia.

Although the fractional excretion of uric acid (FEUA) is known to reflect extracellular fluid volume changes, the diagnostic significance of decreased FEUA in dehydration has not been previously reported. We studied the possible association between low FEUA and acute prerenal azotemia, and its diagnostic value, compared with other traditional indices, in discriminating prerenal azotemia from renal parenchymal causes of acute renal failure. In 65 chronic renal disease patients, 174 FEUA measurements were obtained from 24-hour urine collections. FEUA levels increased as reciprocal serum creatinine levels decreased. All 8 patients with prerenal azotemia showed significantly decreased FEUA values compared with chronic renal disease patients with a comparable degree of serum creatinine elevation, whereas all 7 patients with acute renal failure had FEUA values higher than those of chronic renal disease patients with comparable creatinine levels. FEUA values in prerenal azotemia were distinctly lower than those in acute renal failure (p less than 0.001). Patients with prerenal azotemia showed a lower fractional excretion of sodium, a lower fractional excretion of chloride and renal failure index, and a higher urine-to-plasma creatinine ratio than those with acute renal failure (p less than 0.05). However, these traditional indices were not useful in discriminating between the two conditions. The urine-to-plasma urea nitrogen ratio and the ratio of plasma urea nitrogen to creatinine showed no statistical difference between prerenal azotemia and acute renal failure. We conclude that, in acute azotemia, a decreased FEUA value may represent a reliable indicator of prerenal azotemia in the differential diagnosis of acute renal failure.

Acute Kidney Injury↗
PubMedDate not supplied

Azotemia and mortality among Babesia microti-like infected dogs.

Babesia microti-like piroplasms are a recently recognized cause of illness in dogs in northwest Spain. Our objective was to describe the clinical characteristics and investigate the risk factors for azotemia and death among 58 B microti-like infected dogs. Twenty-one of the 58 (36%) dogs were azotemic at the time that the infection was diagnosed. The case fatality rate during the following week was 22%. Dogs with azotemia at the time of diagnosis were 10 times (95% CI, 3.26-28.8) more likely to die during the following week. Azotemia was the main cause of death for B microti-like infected dogs (attributable fraction = 90%). Severe anemia was present in 45 of the 58 (78%) dogs. Azotemic dogs also presented with hyperphosphatemia, hypoalbuminemia, hypercholesterolemia, proteinuria, and high urine protein: creatinine ratios, suggesting a glomerular component to the disease. Age was the only factor significantly associated with the risk of azotemia (P = .042): on average, a 4-year age increase doubled the risk of an infected dog being azotemic. The only factor significantly associated with mortality was azotemia (P = .001). We concluded that B microti-like infection is associated with a high risk of azotemia and mortality.

Animals↗
PubMed1976

Effect of experimental azotemia on renal clearance of furosemide in the dog.

The clearance of furosemide (F), whose renal tubular transport shares the classical characteristics of the organic acid system, was determined in dogs with varying degrees of azotemia and compared with tetraethylammonium (TEA), an organic base. Two normal and eight azotemic dogs [blood urea nitrogen (BUN), 12-273] were studied. Azotemia was produced by bilateral uretero-venous anastomoses. The left renal vein and ureter were cannulated and renal blood flow (RBF) was measured by electromagnetic flowmeter. Simultaneous left renal clearances (C) of subpharmacological doses of TEA-14C and furosemide-14C were determined at seven 30-minute intervals. Initial loading doses were followed by continuous maintenance infusions. For TEA, clearance (1.5 ml/min-g +/- 0.2 S.E.M.) and extraction (E) (0.83 +/- 0.02) are independent of the degree of azotemia. Renal plasma flow (RPF), calculated as CTEA/ETEA, agreed closely with directly measured RPF (2.0 ml/g-min +/- 0.3). RPF was independent of azotemia. To allow for individual differences in the animals in RPF, the ratio CTEA/CF was used. CF (1.07-0.17 ml/min-g) and EF (0.54-0.06) decreased as a linear function of the increase in uremic serum: (see article). Furosemide and its principle metabolite were greater than or equal to 97% of the furosemide portion of the radioactivity. The metabolite did not increase with time in either plasma or urine. After acute administration of exogenous urea to two dogs (BUN 170 and 253) CTEA/CF was unrelated to BUN. Thus, the CF decreases proportionately with progressive azotemia and is not related to RBF, exogenous urea or metabolite. This suppression of renal tubular secretion of furosemide may partially account for reduced therapeutic efficacy of furosemide in azotemia.

Animals↗
PubMed1980

Azotemia in upper gastrointestinal hemorrhage. A review.

The cause of the azotemia associated with gastrointestinal hemorrhage has been controversial but review of the literature reveals consistent findings. If extraneous, complicating factors are excluded, the azotemia produced with blood ingestion does not reproduce that seen with gastrointestinal hemorrhage. Azotemia with blood ingestion alone demonstrates a mild peak and usually lasts less than 24 hours, whereas that seen clinically is both higher and longer and a manifestation of blood ingestion plus the renal effects of hypovolemia. The hypovolemia contributes quantitatively more than the digestion of blood and is the sole determinant of azotemia after 24 hours. Consequently, azotemia which persists beyond this time indicates either continuation of bleeding, continuation of hypovolemia insult or intrinsic renal disease. Persistent azotemia following gastrointestinal hemorrhage is an indication for re-evaluation of fluid management.

Animals↗
PubMed1996

Prerenal azotemia: differentiation of hyperureagenesis from renal hypoperfusion using urinary urea nitrogen data.

Blood urea nitrogen (BUN) rises disproportionately to serum creatinine in patients with prerenal azotemia whether due to impaired hemodynamics or excessive ureagenesis. To determine whether urinary urea nitrogen excretion rates can distinguish between these caused of hyperuremia we performed a cross-sectional observational study to compare urinary urea nitrogen excretion rates in a highly selected group of patients with prerenal azotemia. Patients who had stable serum creatinine levels, BUN: serum creatinine ratios exceeding 20:1, and progressive azotemia were identified from the hospital laboratory data base. Using conventional clinicolaboratory criteria, 27 patients were diagnosed with either renal hypoperfusion (group I; n = 17) or hyperureagenesis ((group II; n = 10). Random urine sampling for electrolytes, osmolality, creatinine, and urea nitrogen was followed by 24 h collection for creatinine clearance and urinary urea nitrogen. There were no significant differences in age, gender, absolute levels of BUN, or BUN: serum creatinine ratios between the groups. Creatinine clearance (ml/min/1.73 m2) (ml/s/1.73 m2) was lower in group I than in group II (21 +/- 16 vs 36 +/- 13; p < 0.05) (0.35 +/- 0.27 vs 0.60 +/- 0.22; p < 0.05). Twenty-four hour urinary urea nitrogen levels were significantly different (group I, 4.8 +/- 2.9 vs. group II, 13.6 +/- 3.2 gm; p < 0.001) (group I, 171 +/- 300 vs. group II, 486 +/- 114 mmol; p < 0.001). Random urine urea excretion indices were less discriminating but nevertheless still capable of separating the groups. Timed as well as random urine urea nitrogen determinations may assist in differentiating prerenal azotemia due to renal hypoperfusion from hyperureagenesis. Differentiation of these causes of prerenal azotemia might prevent iatrogenic overhydration of patients with azotemia incorrectly attributed to hemodynamic disturbances.

Aged↗
PubMed2003

Gadolinium as a nonnephrotoxic contrast agent for catheter-based arteriographic evaluation of renal arteries in patients with azotemia.

OBJECTIVE: This study was undertaken to determine the effect of gadolinium arteriography on renal function and its diagnostic accuracy in patients with azotemia with suspected renovascular disease. METHODS: Catheter-based digital subtraction arteriographic studies with gadolinium as the contrast agent were performed on 25 occasions in 21 consecutive patients with azotemia to evaluate renal arterial circulation. Gadolinium (gadodiamide, 287 mg/mL) was the only contrast used in these studies. Quantities of gadolinium administered ranged from 40 to 264 mL (mean +/- standard deviation, 124 +/- 74 mL). Serial determinations of renal function were performed in all patients. Arteriography was undertaken 20 times after prior renal revascularizations: seven times as a routine postoperative follow-up study, nine for increasing azotemia, three for worsening hypertension, and once for evaluation of a known renal artery stenosis in patient with an abdominal aortic aneurysm. Three additional arteriograms were performed as part of an evaluation for suspected renovascular hypertension. The two remaining arteriograms were performed in patients with known aortic aneurysms in whom renal artery stenosis was suspected. RESULTS: No adverse changes in renal function followed gadolinium arteriography. Prearteriography serum creatinine values ranged from 1.6 to 9.1 mg/dL (3.0 +/- 1.4 mg/dL), compared with postangiography values that ranged from 1.2 to 8.4 mg/dL (2.9 +/- 1.3 mg/dL). Comparable blood urea nitrogen values ranged from 23 to 71 mg/dL (40.1 +/- 13.5 mg/dL) before arteriography and from 21 to 68 mg/dL (36.5 +/- 13.3 mg/dL) after arteriography. All 38 renal arteries evaluated were adequately imaged. First-order and second-order branchings were well visualized on selective renal studies. Twenty-one renal arteries showed no abnormalities, including six of seven reconstructed arteries subjected to early postoperative evaluation. Twelve renal arteries manifested significant disease, including seven with stenoses and five that had become occluded. Among five additional renal arteries studied, two exhibited obstructing thrombus, two had dissections, and one had a kinked aortorenal bypass graft. CONCLUSION: Catheter-based arteriography in patients with azotemia with gadolinium as a contrast agent is a safe and effective means to evaluate the renal arterial circulation. The preferential use of gadolinium in lieu of nephrotoxic iodinated contrast agents for catheter-based arteriography in patients with azotemia is supported by this experience.

Adult↗
PubMed1984

Hepatic messenger ribonucleic acid activity profiles in experimental azotemia in the rat. Relationship to food intake and thyroid function.

We have studied the hepatic messenger RNA (mRNA) activity profile in chronically azotemic rats and sought to determine whether the observed changes could be mediated either by reduced food intake or diminished thyroid function at the tissue level. mRNA activity profiles were produced by two-dimensional gel electrophoretic separation of radioactively labeled products of an in vitro reticulocyte lysate system which had been programmed by hepatic RNA. Of the approximately 240 translational products identified in this system, seven sequences were consistently altered in azotemia. In pair-fed animals six of these also decreased, but the alterations in three were depressed to a significantly lesser extent in the pair-fed group. Moreover, analysis of covariance suggested that food intake could account for the differences in only one sequence. The possibility that the mRNA activity profile in azotemia could represent the effects of diminished thyroid function was minimized by the finding that the reductions in plasma thyroxine (T4) and triiodothyronine (T3) levels observed were due largely to reduced plasma protein binding, with maintenance of the mean free T4 and free T3 concentrations within the normal range. The changes in only one mRNA sequence could be related to free T3 levels alone. Our findings, therefore, indicate that although diminished food intake and reduced thyroid function may contribute to some of the observed changes in the mRNA activity profiles, the bulk of alterations in azotemia appear to be mediated by other mechanisms. The striking overlap between the sequences affected by azotemia and pair-feeding raises the speculation that altered gene expression in azotemia may reflect an impaired hepatic response at the pretranslational level to metabolic signals associated with food intake.

Animals↗
PubMed2006

Clinical research on navel application of Shehuang Paste combined with Chinese herbal colon dialysis in treatment of refractory cirrhotic ascites complicated with azotemia.

AIM: To explore the efficacy and mechanism of a novel therapeutic method of traditional Chinese medicine in patients with refractory cirrhotic ascites complicated with azotemia. METHODS: Seventy-five cases of refractory cirrhotic ascites complicated with azotemia were randomly divided into 3 groups: comprehensive treatment (n = 29), simple treatment (n = 24), and control (n = 22). The basic treatment methods were the same in all groups, including liver protecting medicines, diuretics and supportive drugs. The control group underwent only the basic treatment. Shehuang Paste (SHP) was applied to the navels of the two treatment groups once a day for 30 d. Colon dialysis with Chinese herbs was administered to the comprehensive treatment group once every two days. Before and after treatment, we measured abdominal circumference, BUN, Cr, serum Na+, urine Na+/K+, liver function, endotoxin content, NO, and ET-1. Color Doppler ultrasonography was conducted to measure the portal vein blood flow. RESULTS: The total effective rate for ascites was 72.4% in the comprehensive treatment group, 45.8% in the simple treatment, contrasting with 18.2% in the controls. Between the two treatment groups and the controls, there were significant differences in the effective rates (P < 0.01, and P < 0.05). There was also a significant difference (P < 0.05) between the two treatment groups. Measurements of Cr and BUN showed higher values for the treatment groups, with the comprehensive better than the simple group (P < 0.05). Sera Na, urine Na/K were different, P < 0.01 between pre- and post-treatment in the comprehensive group, and P < 0.05 in the simple group. The treatment groups' endotoxin content was also significantly reduced (P < 0.01, and P < 0.05), with the comprehensive group better than the simple group (P < 0.05). Portal vein blood flow and NO content significantly reduced (P < 0.05), as did ET-1 content (P < 0.01). There were no significant changes in the control group (P > 0.05). The comprehensive treatment group's pre- and post-treatment portal vein and splenic vein blood flows showed a positive correlation to NO, ET-1 and endotoxin contents. CONCLUSION: When treating refractory cirrhotic ascites complicated with azotemia, Shehuang Paste combined with Chinese herbal dialysis is better than Shehuang Paste alone for ascites resolution, azotemia, and endotoxin elimination. However, both methods on their own were also effective for reducing portal and splenic vein blood flow, and lowering the contents of NO, ET-1 in the two treatment groups.

Administration, Topical↗
PubMed2000

Azotemia (48 h) decreases the risk of brain damage in rats after correction of chronic hyponatremia.

Brain myelinolysis complicates excessive correction of chronic hyponatremia in man. Myelinolysis appear in rats for correction levels deltaSNa) > 20 mEq/l/24 h. We previously showed in rats that when chronic hyponatremia was corrected with urea, the incidence and the severity of brain lesions were significantly reduced compared to hypertonic saline. In man, hyponatremia is frequently associated with azotemia and hemo-dialysis usually corrects rapidly the serum sodium (SNa) but only few patients apparently develop demyelination. We hypothesize that uremic state protects brain against myelinolysis. This hypothesis was evaluated in rats developing azotemia by administration of mercuric chloride (HgCl2, 1.5 mg/kg). Severe (SNa < 120 mEq/l) hyponatremia (3 days) was induced by S.C. AVP and i.p. 2.5% D-glucose for 3 days. HgCl2 was injected on day 2. Hyponatremia was corrected on day 4 by i.p. injections of 5% NaCl in order to obtain a correction level largely above the toxic threshold for brain (deltaSNA approximately 30 mEq/l/24 h). Surviving rats were decapitated on day 10 for brain analysis. In the group with renal failure (Group I, n = 15, urea 59 mmol/l) the outcome was remarkably favourable with only three rats (3/15) dying before day 10 and only one of them (1/3) presenting myelinolysis-related neurologic symptoms. The 12 other rats (80%) survived in Group I without symptoms and brain analysis was normal in all of them despite large correction level (deltaSNa: 32 mEq/l/24 h). On the contrary in nine rats in which HgCl, did not produce significant azotemia (control 1, n = 9, urea: 11 mmol/l), all the rats developed severe neurologic symptoms and eight of them died before day 10. Similar catastrophic outcome was observed in the non-azotemic controls (control 2, no HgCl2 administration, n = 15, urea: 5 mmol/l). All of them developed myelinolysis-related neurologic symptoms and only four of them survived with severe brain lesions (survival 12/15 in Group I vs. 5/24 in pooled controls 1 and 2, p < 0.001). In conclusion, we showed for the first time that chronic hyponatremic rats with azotemia (48 h) tolerated large increases in SNa (approximately 30 mEq/l/24 h) without significant brain damage.

Animals↗
PubMed2002

Massive and disproportionate elevation of blood urea nitrogen in acute azotemia.

In renal failure, blood urea nitrogen and serum creatinine usually rise in tandem; the normal BUN: Cr ratio is 10-15: 1. Disproportionate rises in BUN: Cr (> 20: 1) often imply pre-renal azotemia but may be caused by increased protein catabolism or an excessive protein load. In this study we looked at intensive care patients who acutely developed markedly increased BUN (> or = 100 mg/dL) with only modest elevation of Cr (< or = 5 mg/dL) for possible causes of the disproportionate azotemia. There were 19 such cases collected over 6 months, nine women and ten men, with mean age 69.2 +/- 4.4 years (13/19 > 75 years). Peak BUN was 156 +/- 11 mg/dL; peak Cr 4.3 +/- 0.5 mg/dL. Eleven patients expired. Mean serum albumin at the time of consultation was 2.7 +/- 0.2 g/dL; mean total lymphocyte count 1.0 +/- 0.1/mm3. Of possible factors causing the azotemia, nine patients had documented hypovolemia; eight had congestive heart failure; six were in septic or hypovolemic shock, and two received high-dose steroids. As contributing factors, eight patients had Salb < 2.5 g/dL; eight were given a high protein intake > 100 g/d; two had HIV, and two others had gastrointestinal bleeding. Infection was present in 14 patients; seven had sepsis (bacteremia with hypotension). All patients had at least one of these factors present and 16/19 had two or more. Fractional Na excretion was < 1% (consistent with pre-renal azotemia) in only four of the 11 patients in whom it was measured. We conclude that severely disproportionate BUN : Cr is frequently multifactorial and is most common in the elderly, perhaps due to their lower muscle mass, and in ICU patients given a high protein intake. It is often not indicative of uncomplicated renal hypoperfusion, although low renal perfusion (hypovolemia, shock, or heart failure) is common. Mortality is high due to the severe illnesses, especially infection, worsened by decreased renal function and hypercatabolic state.

Acute Disease↗
PubMed1987

Renal handling of urea in subjects with persistent azotemia and normal renal function.

Fourteen subjects with persistent azotemia and normal glomerular filtration rate were studied by renal clearances and hormonal determinations to establish the nephron site of altered urea transport and the mechanism(s) responsible for their azotemia. During constant alimentary protein, urea nitrogen appearance was normal and urea clearance was much lower than in 10 age-matched control subjects (23.3 +/- 2.1 ml/min and 49.6 +/- 2.6 ml/min per 1.73 m2, P less than 0.001). Inulin and para-aminohippurate clearances, blood volume and plasma concentration of antidiuretic hormone were within normal limits. During maximal antidiuresis, in spite of greater urea filtered load, the urinary excretion of urea was less, and both the maximum urinary osmolality and the free-water reabsorption relative to osmolar clearance per unit of GFR were greater than in control subjects. After sustained water diuresis, the plasma urea concentration markedly decreased to near normal levels in azotemic subjects. The basal urinary excretion of prostaglandins E2 was significantly reduced in azotemic subjects and was directly correlated with fractional urea clearance (r = 0.857, P less than 0.001). An additional group of control subjects (N = 8) showed a marked reduction of fractional clearance of urea after inhibition of prostaglandin synthesis (P less than 0.01). These data suggest that azotemia is due to increased tubular reabsorption of urea in the distal part of nephron, presumably because of increased back diffusion in the papillary collecting duct, accounting for the enhanced maximum urinary osmolality and free-water reabsorption. Renal prostaglandin E2 may participate in the pathogenesis of azotemia by altering recycling of urea in the medulla.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Aluminum intoxication from aluminum-containing phosphate binders in children with azotemia not undergoing dialysis.

Aluminum intoxication developed in three infants with azotemia who were not undergoing dialysis and who had been treated with aluminum hydroxide from the first month of life. Biopsies of the iliac crest demonstrated the presence of severe osteomalacia and massive deposition of aluminum in the bone. Serum aluminum levels were significantly (P less than 0.001) higher in these 3 infants and in 1 other, all of whom received more than 100 mg of elemental aluminum per kilogram of body weight per day (mean +/- S.D., 371.0 +/- 178.9 ng per milliliter [13.75 +/- 6.6 mumol per liter] ) than they were in 8 older children with azotemia who were not undergoing dialysis and who received less than 100 mg of elemental aluminum per kilogram per day (27.0 +/- 18.6 ng per milliliter [1.0 +/- 0.68 mumol per liter] ), 7 such children who did not receive aluminum hydroxide (20.28 +/- 9.2 ng per milliliter [0.75 +/- 0.34 mumol per liter] ), and 16 children with normal renal function (21.04 +/- 4.9 ng per milliliter [0.78 +/- 0.18 mumol per liter] ). In all the children with azotemia who were treated with aluminum hydroxide, there was a positive correlation (r = 0.90; P less than 0.01) between the serum aluminum level and the daily dose of elemental aluminum. These studies indicate that gastrointestinal absorption of aluminum can lead to aluminum intoxication in children with azotemia, and that infants may be particularly susceptible to this complication of therapy.

Adolescent↗
PubMedDate not supplied

Differential effects of direct antagonism of AII compared to ACE inhibitors on serum potassium levels and azotemia in patients with severe congestive heart failure.

OBJECTIVES. The present study was undertaken to determine if direct blockade of angiotensin II receptors by losartan potassium as compared to ACE inhibition might result in greater tolerability in patients with congestive heart failure in whom ACE inhibition resulted in hyperkalemia and azotemia. BACKGROUND. Blockade of angiotensin II receptors by losartan potassium may produce similar benefits in congestive heart failure as ACE inhibition. However, some observations suggest losartan potassium may have different effects on renal function than ACE inhibition. METHODS. Five consecutive patients with severe congestive heart failure were identified in whom treatment with ACE inhibition was complicated by hyperkalemia (K>5.7) and azotemia. In three of these patients losartan potassium was substituted for ACE inhibition while losartan potassium was added to treatment with ACE inhibition in the remaining two. The mean of four serial values of potassium, blood urea nitrogen, and creatinine were compared before and after change in treatment using a two-tailed t test. RESULTS. The addition or substitution of losartan potassium resulted in statistically insignificant reductions in blood urea nitrogen and creatinine and a significant reduction in potassium from 5.7+/-0.1 to 4.9+/-0.3, p<0.03. Two patients who had required kayexalate were withdrawn. In all patients, hyperkalemia resolved and did not reoccur. CONCLUSIONS. There appear to be fundamental differences between the effects of losartan potassium and ACE inhibitors on potassium excretion in congestive heart failure patients with mild to moderate renal insufficiency. Losartan potassium may also be associated with less azotemia in such patients. These differences may have important clinical implications, particularly in the subset of patients in whom ACE inhibition is poorly tolerated as a result of hyperkalemia and azotemia. (c)2000 by CHF, Inc.

Journal Article↗
PubMed1987

Insulin-stimulated protein metabolism in chronic azotemia and exercise.

To determine whether training reduces the acute catabolic stress of an exercise bout, control and azotemic rats, either exercise trained or untrained, were subjected to a bout of exercise or allowed to rest. Protein turnover was measured immediately following exercise in isolated muscles. Azotemia (no exercise) increased protein degradation; acute exercise (no azotemia) decreased protein synthesis. Protein catabolism was greatest in acutely exercised azotemic rats. Training reduced azotemia-induced and acute exercise-stimulated increase in protein degradation. To determine whether this improvement in protein metabolism by training was due to increased insulin sensitivity, the dose-response to insulin was determined. Resistance of protein synthesis or degradation to insulin was not observed in azotemic rats. Either acute exercise or training increased sensitivities of protein degradation and synthesis to insulin; training also increased responsiveness of protein degradation to insulin. Thus exercise training reduced the elevated muscle protein catabolism due to azotemia and/or acute exercise and enhanced the action of insulin on muscle.

Acute Kidney Injury↗
PubMed2006

Diagnostic value of Doppler ultrasound in differentiating prerenal azotemia from acute tubular necrosis in children.

Differentiating acute tubular necrosis (ATN) from prerenal azotemia is critical for selecting the appropriate treatment. This study was conducted to evaluate the diagnostic value of Doppler ultrasonography in differentiating ATN from prerenal azotemia in children. A total of 50 oliguric or anuric children with previous normal renal laboratory data were included. Doppler examination and calculation of resistive index (RI) was performed within 24 hours of admission and in the recovery phase of ARF. The sensitivity and specificity of RI in differentiating ATN from prerenal azotemia were assessed. At the cut-off point of RI = 0.75, the sensitivity and specificity of RI in differentiating prerenal failure and ATN was 91.3% and 85.2%, respectively. We conclude that Doppler ultrasonography is helpful in differentiating ATN from prerenal azotemia in children. The cut-off value of 0.75 has the highest accuracy for this purpose.

Adolescent↗
PubMed1983

Severe reversible azotemia from captopril therapy. Report of three cases and review of the literature.

We saw three cases of severe reversible azotemia secondary to captopril therapy in hypertension. All patients had extensive peripheral vascular disease involving the renal arteries, and two patients (patients 2 and 3) had high levels of peripheral plasma renin activity. The azotemia occurred approximately two weeks after exposure to captopril, and fever, a maculopapular pruritic cutaneous rash, and eosinophilia developed in two patients (patients 2 and 3). The cause of the azotemia in our patients is not clearly known, since renal biopsies were not performed. The most likely cause for the azotemia was volume contraction with reduction in the glomerular filtration rate, although a direct insult to the kidney could not be excluded.

Aged↗