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At least 55 records · Page 3Linked to original sources
PubMed2006

A delayed case of renal artery pseudoaneurysm presented with gross hematuria and azotemia in solitary kidney following percutaneous nephrostomy: treated by transcatheter coil embolization.

Renal arteriovenous fistula or pseudoaneurysms developing after invasive procedures are either asymptomatic or show only transient symptoms. We describe here a case of symptomatic renal artery pseudoaneurysm that presented with gross hematuria and azotemia. The pseudoaneurysm of renal artery was diagnosed by ultrasonography and abdominal magnetic resonance imaging (MRI), and it was successfully treated by percutaneous transcatheter coil embolization. A high index of suspicion is essential for the early diagnosis and treatment of delayed gross hematuria in patients with history of percutaneous nephrostomy.

Aged, 80 and over↗
PubMed1976

Hyperkalemia with cardiac arrhythmia. Induction by salt substitutes, spironolactone, and azotemia.

In two patients, severe hyperkalemia and serious cardiac arrhythmia developed after excessive use of potassium-containing salt substitutes. Both had impaired ability to handle and excrete additional potassium load due to chronic congestive heart failure, azotemia, and administration of spironolactone. Prompt recognition of the arrhythmia and immediate restoration of the cardiac rate and rhythm by pacemaker support followed by intensive regimen to lower the serum potassium prevented a potentially fatal outcome. These cases emphasize the potential danger of salt substitutes when used by patients who are predisposed to retain potassium.

Aged↗
PubMed1977

Depression of renal clearance of furosemide in man by azotemia.

The renal clearance of furosemide and tetraethylammonium (TEA) were compared in 10 patients with hypertensive nephropathy. BUN and creatinine ranges were 10 to 88 mg/dl and 0.9 to 3.8 mg/dl, respectively. Diuretics were discontinued 48 hr prior to the study, and 2 consecutive clearances (ml/min/1.73 m2BSA) of creatinine were performed. The patient then received a bolus followed by a constant infusion of furosemide-14C and tetraethylammonium-14C (analyzed by specific methodology for plasma and urine), both in subpharmacologic doses. After 40-min equilibration sequential 20-min clearance periods were obtained. Both the clearance of furosemide (range 17 to 133) and TEA (range 99 to 443) correlated negatively with BUN and serum creatinine and positively with creatinine and urea clearances. Thus, by using a constant-infusion technique we demonstrated that the renal clearance of furosemide is depressed by azotemia in man and that there was greater depression with furosemide than with TEA.

Adult↗
PubMed1982

Embolization and angioplasty to relieve malignant hypertension and azotemia in a renal transplant patient.

The case of a 23-year-old patient with malignant hypertension following a renal transplant illustrates the successful treatment of the hypertension with embolization of the native kidneys. Azotemia followed and was successfully treated with percutaneous transluminal angioplasty of high-grade stenosis at the anastomotic site of the allograft. Malignant hypertension redeveloped with the recanalization of the embolized native kidneys. This was successfully treated with contrast ablation.

Adult↗
PubMed1996

Management of patients with hemolytic uremic syndrome demonstrating severe azotemia but not anuria.

There are no specific indications for dialysis in a patient with typical hemolytic uremic syndrome (D + HUS) who does not have anuria, hyperkalemia, volume overload, or severe acidemia. We managed five patients with D + HUS, aged 1.5-14 years, without dialysis despite marked azotemia, because they were not anuric and because they had none of the acid-base, fluid, or electrolyte perturbations that may have been indications for dialysis. Each had markedly elevated blood urea nitrogen (range 137-234 mg/dl) and serum creatinine concentrations (range 5.4-15.4 mg/dl). None was anuric and one was oliguric for 4 days. There were no complications and each recovered. We have reviewed the published literature on the use of dialysis in patients with D + HUS and have not found any guidelines that relate to the management of similar cases. It is our view that management of D + HUS patients without dialysis is appropriate when the patient is passing urine and the acid-base, serum electrolyte concentrations and fluid balances can be managed without dialysis.

Adolescent↗
PubMed1982

Diuretic potency of combined hydrochlorothiazide and furosemide therapy in patients with azotemia.

The effect of combined hydrochlorothiazide and furosemide therapy was studied in eight hypertensive patients with renal insufficiency who had poor response to either furosemide or hydrochlorothiazide alone. The study was divided into two parts. In part A, five patients had an inadequate response to furosemide in doses of 160 to 240 mg/day followed a strict protocol in order to compare the effect of increased doses of furosemide with combined hydrochlorothiazide-furosemide administration. All had azotemia, presumable from nephrosclerosis, and had serum creatinine concentrations ranging from 2.3 to 4.9 mg/dl. Four of the five patients had inadequate arterial pressure control, and the remaining patients had fluid retention from the administration of minoxidil. In all five patients, plasma volume was either increased or normal, despite long-term treatment with furosemide. Increasing the dose of furosemide to between 320 and 480 mg/day had only a modest additional diuretic effect, and plasma volume and arterial pressure were not significantly changed. Adding hydrochlorothiazide, 25 to 50 mg twice a day, produced a marked diuresis, and a significant reduction in weight, plasma volume and mean arterial pressure (p less than 0.025 for all three patients). In part B, combined hydrochlorothiazide-furosemide therapy was used to treat three additional patients who had an inadequate response to either diuretic alone. The results indicate that combined hydrochlorothiazide-furosemide is a potent diuretic regimen and is effective in many patients wit chronic renal failure who have a poor response to furosemide alone.

Adult↗
PubMed1985

Vicarious excretion of contrast medium in patients without azotemia.

Although excretion of urographic iodinated contrast agents via the biliary and gastrointestinal tract is not uncommon in patients with renal insufficiency, such vicarious excretion is unusual in the presence of normal renal function. The observation of such vicarious excretion in 2 patients with acute unilateral ureteral obstruction and no azotemia is reported in conjunction with review of the appropriate literature and suggestion of possible etiologies.

Adult↗
PubMed1990

Spurious azotemia associated with 5-fluorocytosine therapy.

A patient with false elevation of serum creatinine level due to 5-fluorocytosine (5-FC) is reported. 5-FC interferes with the enzymatic method used for creatinine determination in the Kodak Ektachem analyzer. Clinicians should be aware of the potential for spurious azotemia in patients receiving 5-FC therapy for fungal urinary tract infections.

Aminohydrolases↗
PubMed1983

Marked azotemia and increase in serum creatinine: case report of an unusual feature of acute ureteral obstruction in a renal allograft recipient.

A patient is described who presented with late ureteral necrosis following renal transplantation, a complication that usually is seen in the early perioperative period. The patient was anuric with azotemia and a high serum creatinine. Response to surgical correction of ureteral obstruction was excellent and renal function returned to normal within 6 days postoperatively.

Adult↗
PubMed1996

Management of postrenal azotemia.

Postrenal azotemia is a potentially life-threatening consequence of urinary obstruction Its most serious consequences include fluid volume deficits, hyperkalemia, and metabolic acidosis. Immediate therapy should be directed at restoring urine flow, correcting extracellular fluid volume deficits, minimizing the cardiac toxicity of hyperkalemia, and ameliorating the cardiovascular effects of metabolic acidosis. Most patients respond quickly and completely to such therapeutic intervention.

Acidosis↗
PubMed1996

Percutaneous renal artery stent placement for hypertension and azotemia: pilot study.

To evaluate the efficacy of balloon-expandable (Palmaz) stents in the treatment of atheromatous renal artery stenosis, prospective placement of stents in 24 arteries in 20 patients was performed over an 18-month period. Indications were hypertension in 18 patients and renal insufficiency (serum creatinine > 1.5 mg/dL) in 11, and all lesions failed conventional transluminal angioplasty. Technical success was achieved in 96% of cases. Hypertension benefit was noted in 77% of patients followed for 6 months (n = 13) and 67% of patients at 1 year (n = 8). Improvement in serum creatinine was seen in 71% (n = 7) and 100% (n = 3) of azotemic patients evaluated at 6 and 12 months, respectively. Six-month angiographic patency was identified in 13 of 16 treated sites. Renal artery stent placement resulted in one asymptomatic segmental branch occlusion; there were no other procedural complications. In conclusion, renal artery stent placement is a technically and clinically effective treatment for hypertension and azotemia due to renal artery stenosis.

Aged↗
PubMed1997

X-linked hypophosphatemia: normal renal function despite medullary nephrocalcinosis 25 years after transient vitamin D2-induced renal azotemia.

Nephrocalcinosis (NC) detected by ultrasound is a recognized abnormality for some patients with X-linked hypophosphatemia (XLH) who received vitamin D2 and inorganic phosphate therapy, but is commonly observed in XLH patients treated with 1,25-dihydroxyvitamin D3 and inorganic phosphate supplementation. Nevertheless, long-term follow-up of kidney function in XLH patients with NC detected ultrasonographically has not been reported. We investigated two women with XLH, ages 31 (patient 1) and 39 (patient 2) years, each of whom had suffered at least one documented episode of vitamin D2-induced hypercalcemia and renal azotemia during childhood. Patient 2 had also been treated with inorganic phosphate. No medications for XLH had been taken during adulthood. Renal ultrasonography at our institution demonstrated marked bilateral medullary NC in both women. No other explanation was found for their NC that apparently occurred several decades earlier from medical therapy for XLH. Detailed studies (including creatinine clearance, beta2-microglobulin excretion, and fasting urinary osmolality and acidification) revealed no impairment of kidney function in either patient. Our findings indicate that subradiographic medullary NC acquired during medical therapy for XLH may persist for decades, but with no adverse renal sequelae. Definitive (long-term) assessment of kidney function in the XLH population with NC, however, will be necessary to fully understand the risk of current medical treatment for this most common heritable form of rickets.

Adult↗
PubMed1990

Novel multivalent effects of pyrazinoylguanidine in patients with azotemia.

In patients with azotemia, urea excretion, urea clearance, and urea/creatinine clearance ratio were increased by pyrazinoylguanidine in a dose-related manner. Urine volume and excretion of sodium greater than chloride greater than potassium tended to increase during administration of pyrazinoylguanidine. Systemic arterial pressure declined while pyrazinoylguanidine was given at 300 or 600 mg b.i.d. for 3 days. At both doses pyrazinoylguanidine reduced plasma renin activity during the first 2 hours. Between days 1 and 3 only the high dose of pyrazinoylguanidine decreased plasma renin activity and plasma aldosterone levels. These findings with pyrazinoylguanidine are consistent with those of secretion of urea in human subjects across the renal tubules and indicate that this process is susceptible to pharmacologic alteration, even in the presence of severe renal insufficiency.

Adult↗
PubMed1987

Acidosis, not azotemia, stimulates branched-chain, amino acid catabolism in uremic rats.

To investigate branched-chain, amino acid metabolism (BCAA) in muscle in chronic renal failure (CRF), we studied rats with moderately severe uremia (PUN 110 approximately mg/dl) and spontaneous metabolic acidosis (bicarbonate, 19 +/- 1 mEq/liter). Plasma BCAA levels in CRF compared to pair-fed control rats were approximately 15% lower and muscle valine was 93 microM lower (P less than 0.05). BCAA metabolism was measured in incubated epitrochlearis muscles using L-[1-14C]valine or L-[1-14C]leucine in the presence and absence of insulin. BCAA decarboxylation was increased (P less than 0.05) and insulin-stimulated BCAA incorporation into protein was blunted (P less than 0.05) by CRF. Since we have found that metabolic acidosis, by itself, stimulates muscle branched-chain, ketoacid dehydrogenase activity, another group of CRF and control rats was given NaHCO3 which corrected the acidosis, but not the azotemia. BCAA decarboxylation in muscle was reduced in CRF rats given NaHCO3, and this was reflected in increased plasma and muscle BCAA concentrations. We conclude that in CRF, chronic metabolic acidosis stimulates BCAA decarboxylation in skeletal muscle and this could contribute to the reduced intra- and extracellular concentrations of BCAA. Correction of acidosis should be a goal of therapy in CRF, especially when dietary regimens restrict intake of BCAA.

Acidosis↗
PubMed1996

Azotemia, TNF alpha, and LPS prime the human neutrophil oxidative burst by distinct mechanisms.

The oxidative burst of neutrophils from azotemic patients (AzoPMNs) is primed for an enhanced response compared to neutrophils from normal subjects (NorPMNs). The mechanism for this priming is unknown, although TNF alpha does not further prime AzoPMNs. The present study examines the hypothesis that azotemia and TNF alpha prime neutrophils by the same mechanism. Formyl peptide receptor expression and degranulation were not primed in AzoPMNs, but were primed by both LPS and TNF alpha. LPS was also able to prime the AzoPMN oxidative burst. Guanine nucleotide exchange by multiple guanine nucleotide binding proteins, including heterotrimeric G-proteins and low molecular weight GTP-binding proteins (LMWGs), was increased in AzoPMNs, as demonstrated by GTP gamma S binding and azidoanilide GTP photoaffinity labeling. The plasma membrane density of G-protein alpha i2, alpha i3, and alpha s subunits and the density in the cytosol of the LMWG, Rap1A, was present in significantly greater amounts on plasma membranes from AzoPMNs. FMet-Leu-Phe-stimulated phospholipase D activity, but not basal activity, was significantly greater in AzoPMNs. Finally, incubation of NorPMNs in plasma from azotemic patients resulted in a significant increase in basal GTP gamma S binding. These results demonstrate that priming of AzoPMNs is restricted to oxidative burst activity and that it occurs by a mechanism distinct from that utilized by TNF alpha and LPS. While the exact mechanism remains unknown, it appears to involve a plasma factor and changes in LMWG expression or activity.

Adult↗
PubMed1997

Azotemia and extrarenal manifestations in old female Han:SPRD (cy/+) rats.

In humans suffering from polycystic kidney disease (PKD) a gender difference is seen with males exhibiting a faster rate of progression of chronic renal failure than females. The aim of this study was to examine renal function in female rats suffering from autosomal dominant PKD [Han:SPRD (cy/+)] and to look for the occurrence of extrarenal organ manifestations of PKD. In young (2 months) as well as in old female rats (21 months) relative kidney weight was greater in affected than unaffected animals. In contrast, only the old affected female rats developed azotemia (serum urea 95 +/- 124 mg/dl) and severe cystic kidney transformation. Furthermore, old affected female rats exhibited liver cysts (affected 42%; unaffected 3%) and pancreatic cysts (affected 69%; unaffected 15%). Liver cyst epithelia stained positive for cytokeratin 19, a marker for bile duct epithelia. By immunohistochemistry liver cysts exhibited a similar extracellular matrix composition as observed in renal cysts of the same animals (staining positive for laminin, fibronectin and heparan sulfate proteoglycan, but not collagen I). This study proves PKD in the Han:SPRD (cy/+) rat model to be a truly multiorgan disease with a close resemblance of the human disease.

Age Factors↗
PubMed2005

Probiotic amelioration of azotemia in 5/6th nephrectomized Sprague-Dawley rats.

The present study was to test the hypothesis that, selected bacteria instilled into the gastrointestinal tract could help in converting nitrogenous wastes accumulated due to renal insufficiency into non-toxic compounds; thereby, ameliorating the biochemical imbalance. Herein we describe a prospective, blinded, placebo controlled pilot-study, using 5/6th nephrectomized Sprague Dawley rat, as a chronic renal failure model. The study group consisted of 36 nephrectomized and 7 non-nephrectomized (control) rats. After two-week nephrectomy stabilization, cohorts of six nephrectomized rats were fed casein-based diet plus one of the following regimens: (A) Control, (B) Placebo (casein-based diet without probiotics), (C) Bacillus pasteurii, (D) Sporolac(R), (E) Kibow cocktail, (F) CHR Hansen Cocktail, and (G) ECONORM. Subsequently, blood (retro-orbital) and urine (collected for measurements of blood urea-nitrogen and creatinine respectively), body weight and bacterial counts (feces) were obtained at regular intervals. The study end-points were to determine if any of the probiotic dietary supplements facilitated, (1) decreased blood concentrations of uremic toxins, (2) altered renal function, and (3) prolonged survival. After 16 weeks of treatment, regimens C and D significantly prolonged the life span of uremic rats, in addition to showing a reduction in blood urea-nitrogen levels, concluding that supplementation of probiotic formulation to uremic rats slows the progression of azotemia, which may correlate with prolonged life span of uremic rats. Derivative trials of probiotic treatment of larger animals and humans will further assess the potential role of probiotic formulations in delaying the onset and clinical severity of clinical illness at different stages of renal failure.

Animals↗
PubMed1982

Fatal reaction following renal angiography and biopsy in diabetic patients with Azotemia.

Severe reactions to contrast media in two diabetic patients with azotemia are described. Both patients also showed signs of immunopathy. The reaction was fatal in one of them. Little is known about contrast media reactions and their natural history. Patients with diabetes mellitus and impaired renal function should be studied with caution and with careful consideration of the indication for the procedure. If an examination with contrast media is considered unavoidable, all diabetic patients with renal failure should be supervised closely to detect the development of acute renal failure. Dehydration should be avoided. Careful monitoring of blood glucose, serum electrolytes, serum creatinine and blood pressure will aid in the early detection of the adverse reaction.

Acute Kidney Injury↗