The lack of clinical value of laboratory parameters in predicting outcome in acute renal failure

In 55 patients with either the oliguric and nonoliguric form of acute renal failure, some laboratory parameters for the analysis of prerenal and intrinsic types of acute renal failure were examined. The parameters were analyzed within 7 days of the clinically known beginning of the illness. The parameters were analyzed as follows: sodium in urine, creatinine urine/plasma ratio, urine osmolality, osmolality urine/plasma ratio, renal failure index, and fractional excretion of filtered sodium. Hemodialysis was performed in 29 of the 55 patients. The oliguric form of acute renal failure was present in 49 of the 55 patients. In relation to renal failure index, prerenal acute renal failure was present in 7 patients and intrinsic acute renal failure in 48. It appears that in patients with a clinical diagnosis of prerenal acute renal failure, the urinary parameters do not separate them from those with acute tubular necrosis. It also appears that in patients with laboratory diagnosis of prerenal acute renal failure (i.e., a RFT less than 1.0), the response to treatment is unpredictable and in fact may have a worse prognosis than in those with a RFI greater than 1.0 (5/7 deaths vs 10/48 deaths).     

Urinary indices in acute interstitial nephritis

Nine patients with biopsy-proven acute interstitial nephritis (AIN) were analyzed for their urinary indices, determined on the basis of the first urinary sample upon admission, before any therapeutic intervention. Isosthenuria was present in all patients with a mean urinary osmolality of 283 +/- 48 mOsm/l and a urine/plasma osmolality ratio of 0.9 +/- 0.1. Urinary sodium was more than 40 mEq/l in 8 out of the 9 patients studied. The other urinary indices studied were indicative for both prerenal and intrinsic renal disease.     

Mortality in Elderly Patients with Acute Renal Failure

In a retrospective study, we identified 55 elderly patients with acute renal failure (ARF) admitted to our hospital during an 8-year period from 1985 to 1993. Information about the etiology, complications, laboratory data, and treatment course were obtained from the clinical history. Of the 200 patients with ARF admitted to the hospital during this period, 28% were patients more than 60 years old (41 male and 14 female) with an average age of 68.5 ± 7 years. The main causes of ARF were sepsis, volume depletion, low cardiac output, arterial hypotension, nephrotoxicity by antibiotics, and obstructive uropathy. The global mortality of elderly patients with ARF was 53%. The mortality rate of the different types of the ARF were: prerenal 35%, intrinsic 64% (oliguric 76%, nonoliguric 50%), and postrenal 40%. Mortality as a result of sepsis occurred in 18 patients (62%), by cardiovascular disease in 4 patients (13%), by acute respiratory failure in 2 patients (7%), and by other causes in 5 patients (18%). In the cases of sepsis, Pseudomonas was detected in 7 cases (39%), Escherichia coli in 2 cases (11%), Gram-negative nonspecific in 3 cases (17%), Klebsiella in 1 case (5%), and in 5 cases (16%), the hemoculture was negative. The patient survival rate was 47% (26 of 55 patients). Of these patients, 19 recovered their normal renal function (73%), but 7 patients remained with renal failure (27%). In conclusion, the global mortality in the elderly patients without considering the types of ARF was 53%. The oliguric form had the highest mortality rate with 76%. The main causes for mortality were sepsis with 62%, cardiovascular disease with 13%, and other causes 18%.     

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.     

Community-acquired acute renal failure

Acute renal failure usually occurs during hospitalization, but may also be present on admission to the hospital. To define the causes and outcomes of community-acquired acute renal failure, we undertook a prospective study of patients admitted to the hospital with acute elevations in serum creatinine concentrations. Over a 17-month period, all admission serum creatinine determinations were screened for patients with values greater than 177 mumol/L (2 mg/dL). These values were compared with baseline creatinines to select patients with an acute elevation in serum creatinine occurring outside the hospital. One hundred patients were entered into the study, with an overall incidence of 1% of hospital admissions. Seventy percent of the patients had prerenal azotemia, 11% had intrinsic acute renal failure, 17% had obstruction, and 2% could not be classified. Mean peak serum creatinine (318 +/- 18 mumol/L [3.6 +/- 0.2 mg/dL]) and mortality (7%) was lowest in the group with prerenal azotemia. In this group, volume contraction due to vomiting, decreased fluid intake, diarrhea, fever, glucosuria, or diuretics was the most common underlying cause. The group with intrinsic acute renal failure had the most severe renal failure and the highest mortality (55%). Although ischemic acute tubular necrosis is the most common cause of hospital-acquired intrinsic acute renal failure, this etiology was seen in only one patient. Drug-induced nephrotoxicity and infection-related causes were the most common underlying etiologies of intrinsic acute renal failure. Obstructive renal failure had a mortality of 24% and was most commonly due to benign prostatic hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Oliguria in patients with normal renal function

Oliguria is common in critically ill patients and may result from prerenal, renal, and postrenal causes. Oliguria also frequently develops in patients with normal concentrations of blood urea nitrogen and creatinine. Most of these patients do not develop renal failure. The authors prospectively studied 100 patients admitted to the ICU to determine the etiology of oliguria in these patients. Eighteen patients (18%) developed oliguria (less than 0.33 ml.kg-1.h-1 X 2 h). Seven and eleven patients were felt on clinical assessment to be hypovolemic or normovolemic, respectively. Compared with the hypovolemic patients, the normovolemic oliguric patients had significantly lower serum osmolalities (278 +/- 3 vs. 290 +/- 5 mOsm/kg H2O) and serum sodium concentrations (138 +/- 3 vs. 132 +/- 1 mEq/l). In addition, normovolemic patients had significantly higher urine sodium concentrations (83 +/- 12 vs. 13 +/- 2 mEq/l), fractional excretion of sodium (1.14 +/- 0.2 vs. 0.15 +/- 0.03), and renal failure indices (1.5 +/- 0.3 vs. 0.21 +/- 0.04). ADH concentrations in six hypovolemic and six normovolemic patients were increased in both groups but not significantly different. The hypovolemic patients increased their urine output from 17 +/- 2 ml/h to greater than 0.5 ml.kg-1.h-1 following a 500-ml bolus of normal saline. The normovolemic oliguric patients remained oliguric following the saline bolus (13 +/- 2 to 19 +/- 3 ml/h). The authors conclude that oliguria is common in critically ill patients and results from renal hypoperfusion and ADH excess.(ABSTRACT TRUNCATED AT 250 WORDS)     

Renal failure with nephrotic syndrome: reversal with large doses of furosemide

The present study documents the occurrence of renal failure in 4 nephrotic patients including 3 with minor glomerular lesions and one with membranoproliferative glomerulonephritis. One patient died of sepsis at 3 months after onset of the acute renal failure. In the remaining 3, forced diuresis employing albumin plus furosemide in increasing doses to 600 mg/day reversed the renal failure independent of corticosteroid therapy. All of the 4 patients showed characteristic findings consisting of a remarkably low fractional excretion of sodium and an unexpectedly low urine osmolality at the onset of acute renal failure, although they were rather hypervolemic. Our findings suggest that the occurrence of a low fractional excretion of sodium and low osmolality may provide a good index of an absolute indication for intensive weight reduction therapy such as high-dose furosemide in nephrotic patients with acute renal failure in order to reverse the acute renal failure.     

Urinary biochemistry in experimental septic acute renal failure.

BACKGROUND: Several biochemical urine tests and derived indices are reported as useful in the diagnosis of acute renal failure (ARF) and its classification in prerenal (hypoperfusion) or intrarenal (acute tubular) necrosis. However, they have not been adequately studied in sepsis, the most frequent cause of ARF in ICU. METHODS: In 10 female Merino ewes, we implanted flow probes around the pulmonary and renal arteries to measure cardiac output and renal blood flow (RBF) continuously. Cardiovascular variables were monitored and urine samples collected during a 48 h control period and one week later during a 48 h period of hyperdynamic sepsis induced by an infusion of live Escherichia coli. RESULTS: Infusion of live E. coli induced systemic hyperdynamic sepsis with renal vasodilatation and increased RBF. Serum creatinine increased from 73.3 +/- 15.1 to 276.9 +/- 156.3 micromol/l (P < 0.05) and creatinine clearance decreased from 84.6 +/- 21.4 to 27.5 +/- 21.4 ml/min (P < 0.05). Urine sodium concentration (UNa) decreased significantly from 164.5 +/- 50.4 to 14.6 +/- 14.3 mmol/l, fractional excretion of sodium (FeNa) from 1.5 +/- 0.17 to 0.12 +/- 0.11%, fractional excretion of urea nitrogen (FeUn) from 62.7 +/- 9.5 to 11.5 +/- 15.4%, and urine osmolality from 724.8 +/- 277.1 mosmol/l to 329.0 +/- 52.1 mosmol/l. The u/p creatinine ratio did not change. CONCLUSION: Sustained Gram-negative sepsis induced a hyperdynamic state and hyperaemic ARF. Despite increased renal perfusion, UNa, FeNa and FeUn decreased significantly. Our findings suggest that, in sepsis, these urinary biochemical changes are not reliable markers of renal hypoperfusion.     

Carbon tetrachloride nephrotoxicity: a reassessment of pathophysiology based upon the urinary diagnostic indices

Inhalation or ingestion of carbon tetrachloride (CCl4) has been said to result in the nephrotoxic lesion of acute tubular necrosis (ATN). We describe three patients who inhaled toxic quantities of CCl4 and presented with oligoanuria and severe hepatoxicity. All patients developed protracted vomiting and were unable to maintain fluid intake for several days prior to our evaluation. Physical examination, urinalysis, and calculated FENa, FEH2O, and renal failure index (RFI) indicated that the acute oliguric renal failure was "prerenal" due to marked extracellular fluid (ECF) volume contraction. Aggressive volume repletion restored renal function to normal in each patient. It is suggested that the acute renal failure following CCl4 exposure begins as a functional disorder and may progress to ATN if volume depletion is not recognized and corrected. Early and aggressive volume repletion will reverse this prerenal state and may prevent the later onset of ATN following CCl4 exposure.     

Nonoliguric acute renal failure

Oliguria has been considered a cardinal feature of acute renal failure. However, many recent reports indicate that acute renal failure usually occurs in the setting of well-maintained urine output. Moreover, the nonoliguric state may accompany acute renal failure due to pre- and post-renal azotemia and a variety of renal parenchymal disorders, as well as acute tubular necrosis. Most studies indicate that nonoliguric forms of acute renal failure are associated with less morbidity and mortality than oliguric acute renal failure. Uncontrolled studies also suggest that volume expansion, potent diuretic agents, and renal vasodilators can convert oliguric to nonoliguric acute tubular necrosis if administered early in the course of acute renal failure. However, prospective studies of early intervention in oliguric patients are needed.     

Plasma renin activity and plasma aldosterone in acute renal failure

Plasma renin activity and plasma aldosterone were determined by radioimmunoassay methods in 20 patients in oliguric phase, in 11 patients in polyuric phase and in 7 patients in convalescent phase of acute renal failure of various origin. The oliguric phase of acute renal failure was characterized by significant increase of plasma renin activity and plasma aldosterone. There was no direct dependence between them. Direct dependence was found between plasma aldosterone and serum potassium in the oliguric phase of acute renal failure, indirect dependence between plasma aldosterone and serum sodium was found before as well as after haemodialysis. These findings prove a direct influence of hyperkalemia and depletion hyponatremia upon aldosterone secretion in the oliguric phase of acute renal failure. Haemodialysis led to a further increase of plasma renin activity caused by ultrafiltration as well as successive dehydration and application of some drugs. The mean value of plasma aldosterone was not significantly changed after haemodialysis. Plasma renin activity decreased very slowly in the polyuric and convalescence phase of acute renal failure, while plasma aldosterone concentration was already in polyuric phase non-significantly different from the control group. There was no direct dependence in the various phases of acute renal failure between plasma renin activity, plasma aldosterone, systolic and diastolic pressure.The renin-angiotensin-aldosterone system significantly participates in the pathogenesis of acute renal failure in man, but various causes of acute renal failure, different drugs, as well as therapeutic procedures do not make it possible to quantify it in detail.Charcoal haemoperfusion in acute poisonings led only to non-significant increase of plasma renin activity and decrease of plasma aldosterone.     

Successful treatment of six patients with neuroleptic malignant syndrome associated with myoglobulinemic acute renal failure

Neuroleptic malignant syndrome is a rare but potentially lethal, rare reaction to neuroleptics which is characterized by altered levels of consciousness, extrapyramidal effects, autonomic instability, hyperthermia, and elevated serum creatine phosphokinase levels. The most serious complication of neuroleptic malignant syndrome is acute renal failure. We investigated six cases of neuroleptic malignant syndrome associated with myoglobulinemic acute renal failure due to rhabdomyolysis and effect of hemodialysis or hemodiafiltration. The patients were five males and one female with a mean age of 43.5 yr. All of the patients, who developed acute renal failure induced from rhabdomyolysis, had previously received butyrophenone (haloperidol), phenothiazine, benzamide, iminomide, benzisoxazole, antidepressants, and hypnotics (benzodiazepine and barbiturate) for the treatment of schizophrenia. The clinical manifestations of neuroleptic malignant syndrome were characterized by altered consciousness, muscle rigidity and weakness, fever, and excessive perspiration. The peak laboratory data were blood urea nitrogen 102 +/- 26 (mean +/- SD) mg/dL, serum creatinine 9.1 +/- 2.1 mg/dL, serum creatine phosphokinase 229,720 +/- 289,940 IU/L, and all of them developed oliguric acute renal failure. Dantrolene sodium administration was given to five cases and hemodialysis or hemodiafiltration was performed in all of them. The serum creatinine level after hemodialysis or hemodiafiltration was 1.4 +/- 1.0 mg/dL. All patients were successfully cured of acute renal failure by hemodialysis or hemodiafiltration. As a result, myoglobulinemic acute renal failure associated with neuroleptic malignant syndrome was successfully treated by hemodialysis or hemodiafiltration.     

Successful Treatment of Six Patients with Neuroleptic Malignant Syndrome Associated with Myoglobulinemic Acute Renal Failure

Neuroleptic malignant syndrome is a rare but potentially lethal, rare reaction to neuroleptics which is characterized by altered levels of consciousness, extrapyramidal effects, autonomic instability, hyperthermia, and elevated serum creatine phosphokinase levels. The most serious complication of neuroleptic malignant syndrome is acute renal failure.

We investigated six cases of neuroleptic malignant syndrome associated with myoglobulinemic acute renal failure due to rhabdomyolysis and effect of hemodialysis or hemodiafiltration.

The patients were five males and one female with a mean age of 43.5 yr. All of the patients, who developed acute renal failure induced from rhabdomyolysis, had previously received butyrophenone (haloperidol), phenothiazine, benzamide, iminomide, benzisoxazole, antidepressants, and hypnotics (benzodiazepine and barbiturate) for the treatment of schizophrenia. The clinical manifestations of neuroleptic malignant syndrome were characterized by altered consciousness, muscle rigidity and weakness, fever, and excessive perspiration. The peak laboratory data were blood urea nitrogen 102 ± 26 (mean ± SD) mg/dL, serum creatinine 9.1 ± 2.1 mg/dL, serum creatine phosphokinase 229,720 ± 289,940 IU/L, and all of them developed oliguric acute renal failure. Dantrolene sodium administration was given to five cases and hemodialysis or hemodiafiltration was performed in all of them. The serum creatinine level after hemodialysis or hemodiafiltration was 1.4 ± 1.0 mg/dL. All patients were successfully cured of acute renal failure by hemodialysis or hemodiafiltration.

As a result, myoglobulinemic acute renal failure associated with neuroleptic malignant syndrome was successfully treated by hemodialysis or hemodiafiltration.     

Significance of the fractional excretion of urea in the differential diagnosis of acute renal failure

BACKGROUND: Fractional excretion of sodium (FENa) has been used in the diagnosis of acute renal failure (ARF) to distinguish between the two main causes of ARF, prerenal state and acute tubular necrosis (ATN). However, many patients with prerenal disorders receive diuretics, which decrease sodium reabsorption and thus increase FENa. In contrast, the fractional excretion of urea nitrogen (FEUN) is primarily dependent on passive forces and is therefore less influenced by diuretic therapy. METHODS: To test the hypothesis that FEUN might be more useful in evaluating ARF, we prospectively compared FEUN with FENa during 102 episodes of ARF due to either prerenal azotemia or ATN. RESULTS: Patients were divided into three groups: those with prerenal azotemia (N = 50), those with prerenal azotemia treated with diuretics (N = 27), and those with ATN (N = 25). FENa was low only in the patients with untreated plain prerenal azotemia while it was high in both the prerenal with diuretics and the ATN groups. FEUN was essentially identical in the two pre-renal groups (27.9 +/- 2.4% vs. 24.5 +/- 2.3%), and very different from the FEUN found in ATN (58.6 +/- 3.6%, P < 0.0001). While 92% of the patients with prerenal azotemia had a FENa <1%, only 48% of those patients with prerenal and diuretic therapy had such a low FENa. By contrast 89% of this latter group had a FEUN <35%. CONCLUSIONS: Low FEUN (相似文献   

Isovolemic hemodialysis combined with hemofiltration in acute renal failure

One hundred cases of servere acute renal failure managed in the intensive care unit were analyzed to assess the value of isovolemic hemodialysis combined with interdialysis hemofiltration to control fluid balance. Forty-five patients were treated prior to the availability of this technique and 55 subsequently. There was a significant reduction in the oliguric period of survivors in the second group compared with the group treated by intermittent hemodialysis alone (p = 0.0459). The significant difference in age between survivors and deaths observed in the first group (p = 0.0027) was not demonstrated in the second group due to a reduction in the incidence of primarily cardiovascular deaths with an improvement in survival of the elderly.     

Are bile acids involved in the renal dysfunction of obstructive jaundice? An experimental study in bile duct ligated rats

BACKGROUND: Surgery on patients with obstructive jaundice is associated with a significant risk of postoperative renal failure. Bile acids are implicated as nephrotoxins because they accumulate in the plasma and the kidney becomes their only excretory route in cholestasis. The experimental evidence favoring this proposal is inadequate and unconvincing. Therefore, we designed an animal experiment involving bile duct ligated (BDL) rats in which we could correlate variations in serum and urine bile acids with indices of nephrotoxicity and renal function. HYPOTHESIS: Bile acids are putative nephrotoxins. MATERIALS AND METHODS: Total serum and urine bile acid concentrations and profiles were determined using liquid chromatography/gas chromatography/mass spectrometry selected ion monitoring. Nephrotoxicity was assessed by renal histopathology and by determination of the urinary activities of the following enzymes: muramidase, glutamate dehydrogenase, alkaline phosphatase, N-acetyl-beta-D-glucosaminidase, and lactate dehydrogenase. Renal function was assessed by measuring urine osmolality, daily osmolar excretion, sodium excretion (U(Na)V), potassium excretion (U(K)V), and total protein and albumin excretion. RESULTS: Maximum plasma concentrations and renal clearance of bile acids occurred between the third or fourth postoperative day following BDL. This peak coincided with maximal disruption of proximal convoluted tubule architecture and postoperative changes in renal function-increased urine flow rate and decreases in urine osmolality and sodium excretion. Thereafter, 1) plasma levels of bile acids returned toward normal levels, 2) urinary bile acid clearance declined, 3) normal renal histology was restored, and 4) normal renal function was reestablished. Throughout this period, fluctuations in enzymuria were evident. However, these shifts did not coincide with plasma and urine bile acid concentrations and histological and functional changes. DISCUSSION AND CONCLUSIONS: Transient functional impairment of renal cation and water transport and nonspecific morphological changes in the proximal convoluted tubule occur 3 to 4 days following bile duct ligation in rats. These functional and morphological changes occurred when plasma total and urinary bile acids were at their peaks. Although it is tempting to equate association with causality, we cannot implicate bile acids as being responsible for the aberrations in renal function and structure following BDL. Accordingly, we have concluded that elevated plasma concentrations of bile acids are renal exacerbates acting in concert with other factors, be they prerenal or renal in origin to precipitate a cascade of events leading to postoperative renal failure in cholestasis.     

Akutes Nierenversagen Pathophysiologie – klinische Beurteilung – Therapie

Acute renal failure (ARF) is characterized by an acute decrease in glomerular filtration rate (GFR). ARF complicates 4% to 23% of intensive care unit admissions, and is associated with a mortality of approximately 50% among critically ill patients. In the intensive care setting the term ARF is usually applied to acute tubular necrosis (ATN), a form of intrinsic ARF caused by ischemia or nephrotoxins. Pathophysiological mechanisms involved in the decline in GFR include tubular obstruction caused by detachment of tubular epithelial cells from the basement membrane and back-leak of glomerular filtrate as a consequence of disruption of the epithelial cell layer. Vascular mechanisms involved in the pathophysiology of ATN are vasoconstriction due to an imbalance between vasoconstrictive and vasodilatory mediators and vascular obstruction caused by cell aggregation. Currently, there is no real time method to monitor renal function comparable to the real time monitoring of blood pressure or arterial oxygen saturation. Urinary output does not reflect glomerular filtration which may be critically reduced despite normal urine volumes and creatinine clearance still provides the clinically most applicable estimate of GFR. Tubular function can be assessed using the fractional excretion of sodium or the ratio of urinary and serum osmolality; both parameters can be obtained from spot samples of urine and serum and no urinary sampling period is necessary. However, both parameters are strongly affected by the administration of loop diuretics and high fluid and sodium inputs which are common in the intensive care unit. We determined the day to day variability of creatinine clearance, fractional excretion of sodium and the urinary to serum osmolality ratio in critically ill patients without renal dysfunction (i.e. creatinine clearance in the normal range) and found differences of 16% for creatinine clearance, 79% for fractional excretion of sodium and 22% for urinary to serum osmolality ratio. Treatment of ARF is mainly supportive and there is no clinically accepted therapy that attenuates the course of ATN. Treatment of the underlying disease and renal replacement therapy are the main options for the treatment of patients with ARF. In critically ill patients continuous venovenous hemo(dia)filtration is the first choice because it provides more hemodynamic and metabolic stability than intermittent therapy. Acute life-threatening hyperkalemia is an indication for intermittent hemodialysis because of the higher efficacy of dialysis in the clearance of low molecular weight substances.     

Renal Functional and Metabolic Studies on the Role of Preventive Measures in Experimental Acute Ischemic Renal Failure

In the present study 1 h of total occlusion of the left renal artery in conscious rats was chosen as experimental model of ischemic acute renal failure (ARF), while the contralateral kidney was left intact. Chronic high dietary sodium intake, acute isotonic saline infusion, or administration of saralasin did not protect from ARF. Furosemide, mannitol, and verapamil converted oliguric into non-oliguric ARF in 100%, 75%, and 60% of the animals, resp. Protection from oliguria and preservation of GFR inversely correlated with the depression of cortical ATP-concentration (control: 1.32 ± 0.07 μmoles/g wet weight) 6 h after ischemia by 16%, 41%, and 58% in mannitol- and verapamil- treated rats and in untreated rats, resp. At this time, Na-K-ATPase enzyme activities in renal cortex and papilla were unaffected, while enzyme activity in outer medulla was suppressed from 15.4 ± 1.4 to 9.4 ± 1.0 μmoles Pi/mg protein h in all groups of animals. The results suggest that in this model of ARF renal ischemia not only affects cellular energy supply in renal cortex but also causes severe structural and functional impairment in the outer medulla, probably leading to tubular obstruction and depression of glomerular function. Pharmacological protection from ischemic oliguric ARF cannot be achieved by prior induction of high urine flow rates alone but depends on the degree of metabolic and functional reserve of the injured tubular epithelium.     

Evaluation of urinary cystatin C as a marker of renal dysfunction

BACKGROUND: Urinary excretion of some low molecular weight proteins (LMWPs) is used as an indicator of tubular dysfunction, since they are increased by the damage of tubular reabsorption. Although serum cystatin C is known to be a sensitive marker for GFR, the property of urinary cystatin C as a LMWP has not been fully observed. We evaluated the clinical utility of urinary cystatin C. METHODS: Urine samples were collected from 130 patients with various degree of renal dysfunction, 62 healthy subjects, and 2 patients with acute renal failure, one with renal acute renal failure, the other with prerenal acute renal failure. Urine levels of cystatin C, beta2-microglobulin (beta2mG), and alpha1-microglobulin (alpha1mG) were measured by immunonephelometry. Creatinine clearance(Ccr) tests were conducted on 130 patients with renal dysfunction. Creatinine(CRE) was measured by enzyme assay. RESULTS: The daily urinary excretions of cystatin C and alpha1mG were increased significantly in patients with Ccr<30 ml/min(group I), compared to those in patients with 30 < or = Ccr<70 ml/min(II), and Ccr > or = 70ml/min(III). Although the mean daily excretion of beta2mG increased as Ccr decreased, the significant difference was not observed. The rate of increase in the mean value between III and I was extremely high in cystatin C. Fractional excretions of cystatin C and beta2mG calculated in the same groups increased significantly in I compared to II and III. The rate of increase in the mean value was higher in cystatin C. Regression analyses between urine CRE and each three LMWP gave the best correlation coefficient for cystatin C in healthy subjects. While in one patient with renal acute renal failure, the rate of increase in urine cystatin C was higher than that of other LMWPs, in another patient with prerenal acute renal failure, the rate of increase in urine cystatin C was low. CONCLUSIONS: Although details of urinary movement of LMWPs in nephrons have not been clearly elucidated, the urinary cystatin C seems to have distinctive properties, and to be useful for the evaluation of renal injury.     

Hypotension,renal failure,and pulmonary complications in leptospirosis

During a recent outbreak of leptospirosis in northeastern Thailand, 148 patients with serologically diagnosed leptospirosis were seen in Loei hospital. The common serotypes were L. pyrogenes, and L. sejroe. Hypotension with a mean arterial pressure less than 70 mmHg upon admission or within 24 h after admission was observed in 94 patients or 64%. 30 patients had normal renal function; 30 patients had prerenal azotemia with mild pulmonary complication in 2; and 34 patients had acute renal failure. 29 patients with acute renal failure had pulmonary complications including pulmonary hemorrhage in 8, pulmonary edema in 3, acute respiratory distress syndrome (ARDS) in 14 and interstitial pneumonitis in 4. 54 patients had normal blood pressure. In this group 5 patients had acute renal failure; 16 had prerenal azotemia and 33 had normal renal function. Interstitial pneumonitis was noted in one patient with prerenal azotemia. Less renal complication and minimal pulmonary complication were seen in leptospirosis patients with normal blood pressure. The patients with normal renal function had no pulmonary complication. Good association existed between hypotension, renal failure and pulmonary complications.