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 469 records · Page 26Linked to original sources
PubMed1999

Risk of transient hyperammonemic encephalopathy in cancer patients who received continuous infusion of 5-fluorouracil with the complication of dehydration and infection.

From 1986 to 1998, 29 cancer patients who had 32 episodes of transient hyperammonemic encephalopathy related to continuous infusion of 5-fluorouracil (5-FU) were identified. None of the patients had decompensated liver disease. Onset of hyperammonemic encephalopathy varied from 0.5 to 5 days (mean: 2.6 +/- 1.3 days) after the initiation of chemotherapy. Plasma ammonium level ranged from 248 to 2387 microg% (mean: 626 +/- 431 microg%). Among the 32 episodes, 26 (81%) had various degrees of azotemia, 18 (56%) occurred during bacterial infections and 14 (44%) without infection occurred during periods of dehydration. Higher plasma ammonium levels and more rapid onset of hyperammonemia were seen in 18 patients with bacterial infections (p=0.003 and 0.0006, respectively) and in nine patients receiving high daily doses (2600 or 1800 mg/m2) of 5-FU (p=0.0001 and < 0.0001, respectively). In 25 out of 32 episodes (78%), plasma ammonium levels and mental status returned to normal within 2 days after adequate management. In conclusion, hyperammonemic encephalopathy can occur in patients receiving continuous infusion of 5-FU. Azotemia, body fluid insufficiency and bacterial infections were frequently found in these patients. It is therefore important to recognize this condition in patients receiving continuous infusion of 5-FU.

Adult↗
PubMed1980

Plasma cell neoplasia with peripheral polyneuropathy. A study of five cases and a review of the literature.

Peripheral polyneuropathy (PPN) is a rare complication of plasma cell neoplasia (PCN), occurring in less than one percent of the patients. Fifty-four such patients (including our 5) were reviewed. There were 42 men (78%) and 12 women (22%) aged 28 to 72 years. Forty-nine percent of patients were younger than 51 years at the time of diagnosis. The initial complaints were different from those observed in multiple myeloma in general, and were related to polyneuropathy in 80% of the patients. PPN was usually of a mixed sensory-motor type and most often involved all four extremities. Skeletal pain was less common than in myeloma in general, occurring initially in 15% and at diagnosis in 45% of the patients. In 21 patients, reversibility of neuropathy was observed. These patients were compared to those with irreversible neuropathy and found to be relatively younger and more aggressively treated with irradiation and modern chemotherapy. Elevated sedimentation rate was uncommon. Less than half of the patients had anemia, and six patients, all with osteosclerotic lesions, had polycythemia. Azotemia was detected in 44% of the cases. No hypercalcemia was observed in 21 examined patients. M components were usually of IgG class, and when the light chains of M components were examined they were invariably of lambda type. Often the level of M component was below 2.0 g/dl. In all patients the bone marrow was infiltrated with immature, abnormal-looking plasma cells, but the infiltrate was often limited to one or a few foci. Solitary plasmacytoma was observed in 14 patients. No anemia, hypercalcemia or azotemia was recorded in this group. Eight patients had serum M components. Bone marrow aspirate was usually normal. In seven patients definite reversibility of PPN was observed after irradiation of plasmacytoma. Twelve patients presented with osteosclerotic lesions (22%), 18 with both osteosclerotic and osteolytic lesions (33%) and 13 with osteolytic lesions. Forty-two percent of the patients had less than three visible lesions in the skeleton. Eleven patients had either osteoporosis or radiologically normal skeleton. The mean survival from the first symptom was about 28 months and from the diagnosis 20 months. The five-year survival was 21% and 20%, respectively. These observations highlight the differences between PCN with PPN and multiple myeloma without PPN.

Adult↗
PubMed1982

Hypertension and primary hyperparathyroidism: a five-year case review.

All cases of surgically proven and cured primary hyperparathyroidism, over a five-year period, were reviewed for the presence of hypertension, renal and/or prerenal azotemia, nephrolithiasis, nephrocalcinosis, and patient symptom status. In this group of 23 patients, the prevalence of hypertension was greater than 78% (18 patients), which is statistically significant. Approximately 28% (5 patients) of the 18 hypertensive patients had some degree of azotemia and/or elevated serum creatinine. Most of the 23 patients were symptomatic, over the age of 50, female, and without nephrolithiasis or nephrocalcinosis. The possible etiologic mechanisms of calcium-mediated hypertension are discussed, and the important association of hypertension with primary hyperparathyroidism is emphasized.

Adenoma↗
PubMed2001

Common iliac artery stenosis presenting as renal allograft dysfunction in two diabetic recipients.

BACKGROUND: Suprarenal common iliac artery stenosis is an uncommon but reversible cause of allograft dysfunction in renal transplant recipients. METHOD: We describe two diabetic renal transplant recipients with worsening hypertension, edema, and azotemia. Magnetic resonance angiography (MRA) demonstrated tight stenoses in the common iliac artery proximal to the allograft anastomosis site with patent renal transplant artery in both cases. These findings were later confirmed with carbon dioxide angiography. RESULTS: No acute rejection was noted on renal biopsy in either case. Placement of percutaneous iliac artery Wallstents resulted in decrease of serum creatinine from 6.5 to 2.0 mg/dl and 1.7 to 1.0 mg/dl within 2 and 4 weeks, respectively. CONCLUSION: Common iliac artery stenosis should be suspected in renal transplant recipients presenting with worsening hypertension, edema and azotemia. MRA for screening followed by carbon dioxide angiography and placement of intravascular stents for focal vascular obstructive lesions reverses allograft dysfunction.

Adult↗
PubMed2000

How to feed patients with renal dysfunction.

Renal dysfunction is common in critically ill patients and its presence has, in the past, posed serious challenges to nutritional support. Such challenges were due to the increased azotemia induced by protein or amino acid administration, the fluid overload caused by the administration of nutrients, and the difficulties associated with the control of these complications by means of conventional dialytic techniques.The development and increasing application of continuous renal replacement therapy has removed such concerns, because control of azotemia and fluid balance can be predictably and reliably achieved in all patients. Accordingly, the presence of renal failure should in no way influence the amount or type of nutritional support administered to a critically ill patient. We recommend that approximately 30-35 kCal/kg/d be administered enterally and begun within the first few hours of admission to the intensive care unit, and that protein intake be kept in the 1.5-2 g/kg/d range.Accumulating evidence also suggest that immune-enhancing enteral preparations decrease the duration of hospital stay, the number of infections, and perhaps mortality. Such preparations should be used in these patients. Finally, adequate vitamin and trace element supplementation is recommended to counterbalance the decrease in antioxidants and the loss of some vitamins during continuous renal replacement therapy. Available evidence suggests that if these steps are applied as part of a protocol-based approach to the nutritional support of patients with renal failure, morbidity and perhaps mortality can be significantly decreased.

Journal Article↗
PubMed2002

Rapid (24-hour) reaccumulation of brain organic osmolytes (particularly myo-inositol) in azotemic rats after correction of chronic hyponatremia.

It was recently demonstrated that renal failure and exogenous urea prevent myelinolysis induced by rapid correction of experimental hyponatremia. To determine why elevated blood urea levels favorably affect brain tolerance to osmotic stress, the changes in brain solute composition that occur when chronic hyponatremia is rapidly corrected were studied in rats with or without mercuric chloride-induced renal failure. After 48 h of hyponatremia, the brains of azotemic and nonazotemic animals became depleted of sodium, potassium, and organic osmolytes. Twenty-four hours after rapid correction of hyponatremia, the brains of animals without azotemia remained depleted of organic osmolytes, with little increase in myo-inositol or taurine contents above those observed in animals with uncorrected hyponatremia; brain electrolytes were rapidly reaccumulated, increasing the brain sodium content to a level 17% higher than values for normonatremic control animals. In contrast, within 2 h after correction of hyponatremia, brain myo-inositol contents in azotemic rats returned to control levels and brain taurine levels were significantly higher than those in azotemic animals with uncorrected hyponatremia (16.5 versus 9 micromol/g dry weight). There was no "overshooting" of brain sodium and water contents after rapid correction in the azotemic animals. Rapid reaccumulation of brain organic osmolytes after correction of hyponatremia could explain why azotemia protects against myelinolysis.

Animals↗
PubMed2004

Allograft diabetic nephropathy may progress to end-stage renal disease.

Mesangial expansion and glomerular basement membrane thickening characteristic of diabetic nephropathy recur in diabetic recipients of renal allografts from non-diabetic donors but progression to renal failure is minimally documented. Three female renal allograft recipients (aged 40, 62 and 73 yr), who developed end-stage renal disease (ESRD) due to recurrent diabetic nephropathy (two patients) and de novo diabetes (one patient) are reported. Onset of proteinuria, uncontrolled hypertension, azotemia, renal allograft pathologic findings and the need for hemodialysis were analyzed. None of the kidney donors (one cadaver, two living related) had known diabetes or perturbed glucose metabolism pre-transplantation. The three patients presented had different varieties of diabetes; type 1, type 2 and new onset diabetes after transplantation (NODAT). In each subject, proteinuria was detected by dipstick at a mean of 8.3 yr (range 8-9) post-transplantation and increased to the nephrotic range (3.7-4.8 g/day) inducing hypoalbuminemia and azotemia. A histopathologic diagnosis of allograft diabetic nephropathy was made in a mean of 11.7 yr (range 10-14), based on glomerular basement membrane thickening, nodular and diffuse intercapillary glomerulosclerosis, arteriolosclerosis, and tubular atrophy with marked tubular basement membrane thickening characteristic of advanced diabetic nephropathy. All three patients manifested uremia and resumed hemodialysis. Two patients died from sepsis within 2 months and one patient died 2.5 yr later after resumption of maintenance hemodialysis. We infer that recurrent or de novo diabetic nephropathy in renal allografts follows a clinical decade-long course irrespective of diabetes. Reports of ESRD due to allograft diabetic nephropathy (ADN) have been limited because of shorter survival of diabetic transplant recipients and few kidney biopsies performed in patients with chronic allograft dysfunction. The occurrence of allograft diabetic nephropathy in some, but not all patients, however, suggests that individual genetic variability modulates disease expression.

Adult↗
PubMedDate not supplied

The effect of combined therapy with captopril, furosemide, and a sodium-restricted diet on serum electrolyte concentrations and renal function in normal dogs and dogs with congestive heart failure.

Captopril, furosemide, and a sodium-restricted diet were administered to 6 normal dogs and 10 dogs with congestive heart failure. Serum electrolyte concentrations and renal function were monitored in both groups. In the normal dogs, no clinically meaningful changes in serum electrolyte, urea nitrogen, or creatinine concentrations developed during therapy with a sodium-restricted diet and 4 weeks each of furosemide alone, captopril alone, or furosemide plus captopril. Three of 6 normal dogs on furosemide and a sodium-restricted diet had at least one serum potassium concentration above the reference range during the 4 weeks of observation. One normal dog on captopril, furosemide, and a sodium-restricted diet developed azotemia, and 2 dogs had serum potassium concentrations above the reference range during the 4 weeks of observation. Ten dogs with congestive heart failure were treated with captopril, furosemide, a sodium-restricted diet, and digoxin. Etiopathogenesis of the heart failure included valvular insufficiency (n = 6), dilated cardiomyopathy (n = 3), and dilated cardiomyopathy and dirofilariasis (n = 1). Serum electrolyte concentrations and renal function were monitored for 5 consecutive weeks in 7 of the 10 dogs and for 17 weeks or longer in 6. Two dogs were euthanized after 4 weeks because of acute decompensation of heart failure, and one dog developed severe azotemia and uremia. Six of 10 dogs with congestive heart failure had at least one serum potassium concentration above the reference range sometime during the 5 weeks of observation, although the changes in the mean serum potassium concentrations were not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Resolution of a left ureteral stone using electrohydraulic lithotripsy in a thoroughbred colt.

A 3-year-old Thoroughbred colt was presented for evaluation of azotemia and anorexia. Physical examination revealed a ureterolith in the left ureter, approximately 10 cm from the bladder, which was thought to obstruct urine flow by approximately 90% when viewed cystoscopically. Ultrasonographic examination of both kidneys revealed indistinct corticomedullary junctions, and the right kidney was more hyperechoic. A percutaneous biopsy of the right kidney revealed chronic interstitial nephritis with marked interstitial medullary fibrosis. Medical therapy consisting of IV fluids, sodium chloride PO, and ammonium chloride PO was initiated. Ureteroscopic electrohydraulic lithotripsy via a perineal urethrostomy was used to successfully remove the stone. Klebsiella oxytoca, which responded to oral enrofloxacin therapy, was cultured from the urine after surgery. Azotemia resolved and the horse resumed training.

Animals↗
PubMed1998

Rhesus macaques infected with macrophage-tropic simian immunodeficiency virus (SIVmacR71/17E) exhibit extensive focal segmental and global glomerulosclerosis.

We previously showed that inoculation of rhesus macaques with molecularly cloned lymphocytetropic simian immunodeficiency virus (SIVmac239) results in SIV-associated nephropathy (SIVAN) and that the glomerulosclerotic lesions were associated with the selection of macrophagetropic (M-tropic) variants (V. H. Gattone et al., AIDS Res. Hum. Retroviruses 14:1163-1180, 1998). In the present study, seven rhesus macaques were inoculated with M-tropic SIVmacR71/17E, and the renal pathology was examined at necropsy. All SIVmacR71/17E-infected macaques developed AIDS, and most developed other systemic complications, including SIV-induced encephalitis and lentivirus interstitial pneumonia. There was no correlation between the length of infection (42 to 97 days), circulating CD4(+) T-cell counts, and renal disease. Of the seven macaques inoculated with SIVmacR71/17E, five developed significant mesangial hyperplasia and expansion of matrix and four were clearly azotemic (serum urea nitrogen concentration of 40 to 112 mg/dl). These same five macaques developed focal segmental to global glomerulosclerotic lesions. Increased numbers of glomerular CD68(+) cells (monocytes/macrophages) were found in glomeruli but not the tubulointerstitium of the macaques inoculated with SIVmacR71/17E. All macaques had glomerular deposits of immunoglobulin G (IgG), IgM, and tubuloreticular inclusions, and six of seven had IgA deposition. However, there was no correlation between the presence of circulating anti-SIVmac antibodies, immunoglobulin deposition, and glomerular disease. Tubulointerstitial infiltrates were mild, with little or no correlation to azotemia, while microcystic tubules were evident in those with glomerulosclerosis or azotemia. The four most severely affected macaques were positive for diffuse glomerular immunostaining for viral core p27 antigen, and there was intense staining in the glomeruli of the two macaques with the most severe glomerulosclerosis. Viral sequences were isolated from glomerular and tubulointerstitial fractions from macaques with severe glomerulosclerosis but only from the tubulointerstitial compartment of those that did not develop glomerulosclerosis. Interviral recombinant viruses generated with env sequences isolated from glomeruli confirmed the M-tropic nature of the virus found in the glomeruli. The correlation between the increased number of CD68(+) cells (monocytes/macrophages) in the glomeruli, the localization of p27 antigen in the glomeruli, and the glomerular pathology confirms and extends our previous observations of an association between glomerular infection and infiltration by M-tropic virus and SIVAN.

AIDS-Associated Nephropathy↗
PubMed1991

Acute renal failure: possible role of duplex Doppler US in distinction between acute prerenal failure and acute tubular necrosis.

Ultrasonography (US) of the native kidneys is commonly requested for acute renal failure (ARF), although in most cases the examination results are negative. To detect changes in the Doppler waveform associated with ARF and determine whether Doppler US can provide significant diagnostic information not available with standard US, 91 patients with ARF were studied to determine a mean resistive index (RI) for each patient. Forty-six patients had acute tubular necrosis (ATN) with a mean RI +/- 1 standard deviation of .85 +/- .06, which was significantly higher than the mean RI of .67 +/- .09 in 30 patients with prerenal ARF (P less than .01). Fifteen patients had ARF due to non-ATN intrinsic renal disease (mean RI, .74 +/- .13). An elevated RI (greater than or equal to .75) occurred in 91% of patients with ATN versus only 20% of patients with prerenal azotemia. Patients with severe liver disease (hepatorenal syndrome) are a subset of those with prerenal ARF that accounted for most of the elevated RIs in this group. The study demonstrates that intrarenal Doppler US allows detection of changes associated with ARF far more often than standard US. More important, Doppler US may be helpful in distinguishing ATN from prerenal azotemia.

Acute Kidney Injury↗
PubMed1986

Escherichia coli endotoxin injections potentiate experimental ischemic renal injury.

UNLABELLED: The purpose of this study was to assess the influence of Escherichia coli endotoxin on the evolution of ischemic acute renal failure (ARF). Rats were subjected to 25 min of bilateral renal artery occlusion (RAO) plus subcutaneous/intraperitoneal injections of either boiled E. coli or purified E. coli endotoxin (1.5 mg). Boiling the E. coli renders them nonviable but leaves endotoxin intact. Ischemic controls were injected with saline. The E. coli injections exacerbated ischemic ARF, doubling the degree of azotemia and increasing the extent of tubular necrosis and cast formation. This occurred without an adverse effect on renal blood flow or blood pressure during the initiation phase or maintenance phase of the ARF. Endotoxin tolerant rats were totally protected against the E. coli-ARF potentiating effect. Neither Staphylococcus aureus nor E. coli with denatured endotoxin adversely affected ischemic injury. Purified E. coli endotoxin reproduced the E. coli-ARF potentiating action. Neither E. coli nor purified endotoxin induced azotemia in the absence of renal ischemia. CONCLUSION: E. coli endotoxin can exacerbate ischemic renal injury without compromising renal hemodynamics. This action appears to be mediated by an adverse effect of endotoxin on critical subcellular determinants of ischemic tissue injury.

Acute Kidney Injury↗
PubMed2002

How to feed patients with renal dysfunction.

Renal dysfunction is common in critically ill patients and its presence has, in the past, posed serious challenges to nutritional support. Such challenges were due to the increased azotemia induced by protein or amino acid administration, the fluid overload caused by the administration of nutrients and the difficulties associated with the control of these complications by means of conventional dialytic techniques. The development and increasing application of continuous renal replacement therapy (CRRT) has removed such concerns, because control of azotemia and fluid balance can be predictably and reliably achieved in all patients. Accordingly, the presence of renal failure should in no way influence the amount or type of nutritional support administered to a critically ill patient. We recommend that approximately 30-35 kcal/kg/day be administered enterally and begun within the first few hours of admission to the intensive care unit and that protein intake be kept in the 1.5-2 g/kg/day range. Accumulating evidence also suggests that immune-enhancing enteral preparations decrease the duration of hospital stay, the number of infections and perhaps mortality. Such preparations should be used in these patients. Finally adequate vitamin and trace element supplementation is recommended to counterbalance the decrease in antioxidants and the loss of some vitamins during CRRT. Available evidence suggests that if these steps are applied as part of a protocol-based approach to the nutritional support of patients with renal failure, their morbidity and perhaps mortality can be significantly decreased.

Amino Acids↗
PubMed1987

Prognosis of the nephrotic syndrome in sickle glomerulopathy. A retrospective study.

Of 240 adults with sickle cell anemia seen over 11 years, 12 had the nephrotic syndrome. In 9 (75%) the glomerular lesion, sickle glomerulopathy, consisted of mesangial expansion and basement membrane duplication. Six patients had type IV renal tubular acidosis. Four of the 9 Patients died within 24 months (17 +/- 5; mean +/- SD), while 5 survived 36 months or longer (80 +/- 49); no significant differences were seen between the former and the latter in age, admission serum creatinine and C3 levels, urinary protein excretion, or the frequency of renal tubular acidosis. Chronic azotemia developed in 3 and acute renal shutdown in another 2. Of 22 patients with sickle glomerulopathy (our 9 added to 13 from the literature) 11 died within 2 years. Ten of these (91%) had developed renal failure, compared to only 5 of the 11 (45%) who survived longer than 2 years (p less than 0.05). The 5-year mortality in the general population of sickle cell anemia is 3.75%, and 75% of patients aged 15 years or older survive 18 years or longer. The nephrotic syndrome, most often caused by sickle glomerulopathy, occurs in 4% of patients with sickle cell anemia, leading to renal failure in two-thirds and death in 2 years in half the patients. The development of chronic azotemia correlates strongly with early mortality. The prognosis is much worse than that in the general population of sickle cell anemia.

Adult↗
PubMed1988

Suction-supported continuous arteriovenous hemofiltration in children.

Spontaneous continuous arteriovenous hemofiltration (CAVH) may fail to control azotemia in small patients with renal failure due to poor blood flow. To produce adequate ultrafiltrate a continuous negative pressure was added to the ultrafiltrate line. Two hemofilter systems of different membrane and surface area were used. Suction support approximately doubled ultrafiltration rate in both hemofilters. No side effects such as severe hypotonia or early hemofilter clotting occurred. Added suction can serve as a useful support of spontaneous CAVH in children with renal failure and too poor a blood flow to control azotemia.

Acute Kidney Injury↗
PubMed1991

Treatment of azotemic, nonoliguric, anemic patients with human recombinant erythropoietin raises whole-blood viscosity proportional to hematocrit.

It has been reported that patients with azotemia have reduced red blood cell (RBC) deformability. Since this is a major determinant of whole-blood viscosity (WBV) and rigid RBCs increase WBV disproportionately relative to the level of hematocrit, it is conceivable that sustained improvement of hematocrit with recombinant human erythropoietin (rhEPO) therapy in azotemic patients might result in abnormally raised WBV. To address this concern, WBV and plasma viscosity (PV) were measured in 9 adult patients (4 men, 5 women) with anemia (mean hematocrit 29.2 +/- 2.7%) and azotemia [mean serum creatinine concentration 339.85 +/- 102.44 mumol/l (3.8 +/- 1.1 mg/dl)] before and after 6 months of treatment with rhEPO (50-175 U/kg given intravenously thrice weekly). Baseline and post-treatment hematocrit, WBV and PV were compared to values derived in 50 normal adult subjects with normal renal function [25 women, 25 men; mean serum creatinine concentration 79.56 +/- 8.84 mumol/l (0.9 +/- 0.1 mg/dl), mean hematocrit 42.4 +/- 3.7%]. To compare rheologic factors at subnormal hematocrits, blood from subjects with normal renal function was diluted with autologous plasma to achieve a range of hematocrits from 20 to 50%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Effects of converting enzyme inhibition on split renal function in renovascular hypertension.

The effects of captopril on effective renal plasma flow and glomerular filtration rate were studied using a noninvasive radioisotopic method on individual kidneys in eight patients with renovascular hypertension and 12 patients with essential hypertension with various renin levels. Four patients with renovascular hypertension had unilateral while three had bilateral renal artery stenosis. The effective renal plasma flow and glomerular filtration rate were determined by using 131I-iodohippurate sodium and 99mTc-diethylenetriamine pentaacetic acid, respectively. Glomerular filtration rate and effective renal plasma flow were significantly reduced in the stenotic kidneys of patients with renovascular hypertension compared with values in nonstenotic kidneys (p less than 0.01). Treatment with captopril, 37.5 to 75 mg/day for 1 to 48 weeks, further reduced the glomerular filtration rate only in stenotic kidneys, and effective renal plasma flow increased in both kidney types. In two of the three renal hypertensive patients with bilateral renal artery stenosis, captopril produced a reversible azotemia that was unrelated to the fall in blood pressure, as evidenced by the lack of azotemia seen after a moderate blood pressure reduction induced by other antihypertensive medications. These results indicate that endogenous angiotensin II is essential in maintaining the glomerular filtration rate in stenotic kidneys and suggest that a reduction in glomerular filtration rate during captopril administration could indicate the presence of renal artery stenosis.

Adult↗
PubMed1976

The vascular basis for acute renal failure in the rat. Preglomerular and postglomerular vasoconstriction.

Myohemoglobinuric acute renal failure (ARF) was induced in dehydrated, salt-deficient, salt-loaded, and untreated rats by intramuscular injection of glycerol, and the renal vasculature was studied after 24 hours. Kidneys were prepared for examination by rapid freezing in vivo to -160 degrees C and freeze substitution in -80 degrees C alcohol, and by perfusion fixation with 1% glutaraldehyde in Ringer's solution at 120 mm Hg. Frozen kidneys were examined by light microscopy after paraffin and epoxy resin embedding. Techniques used in examining the perfusion-fixed kidneys were: (1) vascular injection with silicone rubber and clearing in glycerol, (2) electron microscopy, and (3) morphometric evaluation of lumen to wall area ratios of glomerular arterioles. Kidneys of all rats with ARF showed renal cortical arterial and glomerular arteriolar (afferent and efferent) vasoconstriction. The degree of constriction, estimated by lumen to wall ratios, correlated with the degree of azotemia (r = -0.71; P less than 0.001). Differences between all ARF groups and respective controls were highly significant (P less than 0.001). Vasoconstriction was maximal in the dehydrated group, intermediate in the untreated and Na-deficient rats, and lowest in the salt-loaded animals. Glomerular and peritubular capillaries were patent and free of endothelial swelling or thrombi. Glomerular basement membranes and epithelial foot processes showed no morphological alterations. The observations suggest that marked pre- and postglomerular vasoconstriction occurs in established myohemoglobinuric ARF, that it is related to azotemia, and that mechanical vascular obstruction does not play a major role in this experimental model.

Acute Kidney Injury↗