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Acute renal failure in blacks and Indians in South Africa--comparison after 10 years.

Acute renal failure (ARF) has changed in its aetiology in developed Western countries. This study compares our experiences of the aetiology and incidence of ARF a decade after a previously recorded paper in the literature. The data of 226 patients with a diagnosis of ARF during a 3-year period from 1986 to 1988 was analysed. ARF in our study occurred at a younger age. Medical causes of ARF remain the dominant subgroup. There were female patients presenting with ARF associated with self-induced abortions. Toxins of a herbal variety and infections remain the commonest aetiological factors in the medical subgroup. Infections have replaced nephrotoxins as being the principal medical cause. There has been no major change in the incidence or aetiology of ARF over a decade. The prevention of ARF in blacks in sub-Saharan Africa is primarily concerned with the eradication of nephrotoxins and infections and a laxity in the abortion laws of the country. Only by an improvement in education, nutrition, socio-economic status and sanitation can one eradicate or diminish ARF in developing countries.

Acute Kidney Injury↗

Neurodiagnostic abnormalities in patients with acute renal failure.

Neurological abnormalities are a major cause of morbidity in patients with renal failure. The pathophysiology of these neurological changes is unclear, and the effects on them of dialysis and return of renal function have not been well studied. Studies were done in 31 patients who had acute renal failure (ARF), all of whom were either treated with dialysis within 5 days or did not survive. Studies on these patients included the electroencephalogram (EEG), motor nerve conduction velocity, and plasma Ca(++) and parathyroid hormone (PTH) levels. Studies were done at the time ARF was diagnosed, after stabilization on dialysis, during the diuretic phase of ARF, and 3 mo after recovery from ARF. In 16 patients with acute or chronic renal failure who did not survive and in nine patients without renal disease who died, measurements were made in brain of content of Na(+), K(+), Cl(-), Ca(++), Mg(++), and water. In patients with ARF for less than 48 h, despite the fact that there were only modest increases in plasma urea and creatinine, there were striking abnormalities in the EEG. The percent EEG power < 5 Hz+/-SE was 41+/-8% (normal = 2+/-1%), whereas the percent of frequencies > 9 Hz was only 22+/-6% (normal = 62+/-3%). These changes were unaffected by dialysis, but became normal with return of renal function and remained normal at 3 mo follow-up. The motor nerve conduction velocity was unaffected by either ARF or dialysis. In patients with ARF, the brain Ca(++) was 46.5+/-3.2 meq/kg dry wt, almost twice the normal value of 26.9+/-1.0 meq/kg dry wt (P < 0.001). The plasma PTH level was 3.2+/-0.6 ng/ml (normal < 1.5 ng/ml, P < 0.01). The increased brain Ca(++) was not related to an increased plasma (Ca(++)) (PO(4) (---)) product (r(2) = 0.14, P > 0.05). There was a small but significant decrement in brain Na(+) (P < 0.05), but brain water, K(+), and Mg(++) were unaffected by ARF.Thus, in patients with ARF for less than 48 h, the EEG is grossly abnormal and there are elevated levels of PTH in plasma. The PTH appears to have a direct effect on the brain, resulting in an increased brain Ca(++) content. The EEG abnormalities are unaffected by dialysis, but they become normal with return of renal function and remain normal after 3 mo follow-up. Thus, PTH may be a major uremic toxin, demonstrating evidence for central nervous system toxicity when there are only minimal abnormalities of other biochemical markers of ARF.

Acute Kidney Injury↗

Increased nitric oxide synthase activity despite lack of response to endothelium-dependent vasodilators in postischemic acute renal failure in rats.

Lack of response to endothelium-dependent vasodilators generally has been considered to be evidence for decreased nitric oxide synthase (NOS) activity and NO generation after ischemic or hypoxic injury to vital organs including the kidney. In this study, renal blood flow (RBF) responses to endothelium-dependent vasodilators acetylcholine and bradykinin and the endothelium-independent vasodilator prostacyclin, the nonselective NOS inhibitor L-NAME (without and with L-arginine), the inducible NOS inhibitor aminoguanidine, and the NO-donor sodium nitroprusside were examined in 1-wk norepinephrine-induced (NE) and sham-induced acute renal failure (ARF) rats. Compared with sham-ARF, there was no increase in RBF to intrarenal acetylcholine and bradykinin, but a comparable RBF increase to prostacyclin in NE-ARF kidneys. However, there was a significantly greater decline in RBF to intravenous L-NAME in NE- than sham-ARF rats (-65 +/- 8 vs. -37 +/- 5%, P < 0.001) which was completely blocked by prior L-arginine infusion. There was no change in RBF to the inducible NOS specific inhibitor aminoguanidine. Unlike sham-ARF, there was no increase in RBF to intrarenal sodium nitroprusside in NE-ARF. Immunohistochemistry and immunofluorescence detection of constitutive (c) NOS using mouse monoclonal antibody were carried out to positively determine the presence of cNOS in NE-ARF. 90% of renal resistance vessels showed evidence of endothelial cNOS in both sham- and NE-ARF. Taken together, results of these experiments are consistent with the conclusion that NOS/NO activity is, in fact, maximal at baseline in 1-wk NE-ARF and cannot be increased further by exogenous stimuli of NOS activity. The increased NOS is likely of the constitutive form and of endothelial origin. It is suggested that the increased NOS activity is in response to ischemia-induced renal vasoconstrictor activity. Attenuated response to endothelium-dependent vasodilators cannot be interpreted only as evidence for decreased NOS activity.

Acetylcholine↗

Impaired IL-18 processing protects caspase-1-deficient mice from ischemic acute renal failure.

We sought to determine whether mice deficient in the proinflammatory caspase-1, which cleaves precursors of IL-1 beta and IL-18, were protected against ischemic acute renal failure (ARF). Caspase-1(-/-) mice developed less ischemic ARF as judged by renal function and renal histology. These animals had significantly reduced blood urea nitrogen and serum creatinine levels and a lower morphological tubular necrosis score than did wild-type mice with ischemic ARF. Since caspase-1 activates IL-18, lack of mature IL-18 might protect these caspase-1(-/-) mice from ARF. In wild-type animals, we found that ARF causes kidney IL-18 levels to more than double and induces the conversion of the IL-18 precursor to the mature form. This conversion is not observed in caspase-1(-/-) ARF mice or sham-operated controls. We then injected wild-type mice with IL-18-neutralizing antiserum before the ischemic insult and found a similar degree of protection from ARF as seen in caspase-1(-/-) mice. In addition, we observed a fivefold increase in myeloperoxidase activity in control mice with ARF, but no such increase in caspase-1(-/-) or IL-18 antiserum-treated mice. Finally, we confirmed histologically that caspase-1(-/-) mice show decreased neutrophil infiltration, indicating that the deleterious role of IL-18 in ischemic ARF may be due to increased neutrophil infiltration.

Acute Kidney Injury↗

Neutrophil-independent mechanisms of caspase-1- and IL-18-mediated ischemic acute tubular necrosis in mice.

Having recently described the injurious role of caspase-1-mediated production of the proinflammatory cytokine IL-18 in ischemic acute renal failure (ARF), we report here on the effect of the newly developed caspase inhibitor Quinoline-Val-Asp(Ome)-CH(2)-OPH (OPH-001) on caspase-1, IL-18, neutrophil infiltration, and renal function in ischemic ARF. C57BL/6 mice with ischemic ARF treated with OPH-001 had a marked (100%) reduction in blood urea nitrogen (BUN) and serum creatinine and a highly significant reduction in morphological acute tubular necrosis (ATN) score compared with vehicle-treated mice. OPH-001 significantly reduced the increase in caspase-1 activity and IL-18 and prevented neutrophil infiltration in the kidney during ischemic ARF. To evaluate whether this lack of neutrophil infiltration was contributing to the protection against ischemic ARF, a model of neutrophil depletion was developed. Neutrophil-depleted mice had a small (18%) reduction in serum creatinine during ischemic ARF but no reduction in ATN score despite a lack of neutrophil infiltration in the kidney. Remarkably, caspase-1 activity and IL-18 were significantly increased in the kidney in neutrophil-depleted mice with ARF. In addition, IL-18 antiserum-treated neutrophil-depleted mice with ischemic ARF had a significant (75%) reduction in serum creatinine and a significant reduction in ATN score compared with vehicle-treated neutrophil-depleted mice. These results suggest a novel neutrophil-independent mechanism of IL-18-mediated ischemic ARF.

Amino Acid Chloromethyl Ketones↗

Evaluation of factors to decrease bioavailability of cyclosporin A in rats with gentamicin-induced acute renal failure.

Focusing on the disposition of cyclosporin A (CsA) in the liver and intestine, effects of gentamicin-induced acute renal failure (ARF) on the decreased oral bioavailability of CsA were evaluated in rats. The area under the CsA concentration-time curve (AUC) in ARF rats after oral administration (5 mg/kg) significantly decreased by 43% as compared to the control, while the apparent oral clearance significantly increased by 76% of the control. The portal AUC of CsA in ARF rats with bile flow decreased by 67% as compared to the control rats. Without bile flow, the portal AUC of CsA in control rats decreased by 50% as compared to those with bile flow, whereas ARF rats without bile flow showed no notable change as compared to those with bile flow. The AUC of CsA mono-oxidative metabolite via CYP3A (M-OH) in ARF rats after oral or intravenous administration increased significantly by 84% or 241%, respectively, while there was no difference in the portal M-OH between control and ARF rats, suggesting that the elimination of M-OH was prolonged because of nephrotoxicity. Although the exsorption clearance of CsA from the blood circulation to the intestine after intravenous administration to ARF rats decreased significantly as compared to the control; and basolateral-to-apical transport of CsA through Caco-2 monolayers was significantly retarded in the presence of uremic toxins, there was no significant change in the total body clearance of CsA between ARF and control rats. Moreover, there were no effects of uremic toxins on the protein binding of CsA in plasma. These observations suggest that hepatic or intestinal CYP3A and P-glycoproteine (P-gp) are not likely to be concerned with lowering the oral bioavailability of CsA, and that bile function under the ARF condition induced by gentamicin is responsible for a marked decrease in the fraction absorbed of CsA in the small intestine.

Acute Kidney Injury↗

Prevention of acute renal failure.

Acute renal failure (ARF) comprises a family of syndromes that is characterized by an abrupt and sustained decrease in the glomerular filtration rate. In the ICU, ARF is most often due to sepsis and other systemic inflammatory states. ARF is common among the critically ill and injured and significantly adds to morbidity and mortality of these patients. Despite many advances in medical technology, the mortality and morbidity of ARF in the ICU continue to remain high and have not improved significantly over the past 2 decades. Primary strategies to prevent ARF still include adequate hydration, maintenance of mean arterial pressure, and minimizing nephrotoxin exposure. Diuretics and dopamine have been shown to be ineffective in the prevention of ARF or improving outcomes once ARF occurs. Increasing insight into mechanisms leading to ARF and the importance of facilitating renal recovery has prompted investigators to evaluate the role of newer therapeutic agents in the prevention of ARF.

Acetylcysteine↗

Hospital survival rates of patients with acute respiratory failure in modern respiratory intensive care units. An international, multicenter, prospective survey.

An international, multicenter, prospective survey has been conducted to determine the hospital survival rates of patients with potentially reversible acute respiratory failure (ARF) who are managed in sophisticated intensive care units by leading critical care specialists, using current (1991 to 1992) support and treatment techniques and protocols. Twenty-five clinical centers participated in the survey, 11 in the United States and 14 in Europe. A total of 1,426 patients with ARF were studied, all of whom had been receiving closed system positive pressure mechanical ventilation at an FIo2 of at least 0.50 for at least 24 h at the time of entry into the survey. Of the survey patients, 793 (55.6%) survived their hospitalization, while 633 (44.4%) died in the hospital. The 1,426 patients with ARF were prospectively divided into two groups: group A, containing 375 patients, who at the time of entry into the study were hypoxemic or hypercarbic while receiving mechanical ventilator assistance; and group B, containing 1,051 patients, who at the time of entry into the study were neither hypoxemic nor hypercarbic while receiving mechanical ventilator support at an FIo2 of 0.50 or greater. Hospital survival rate for group A patients was 33.3% and for group B patients it was 63.6%. Survival rates were higher in patients with ARF caused by pneumonia (63%) or post shock lung injury (67%) and lower in patients with ARF caused by sepsis (46%). Severity of lung injury at the time of entry into the survey was a major prognostic factor, varying from an 18% hospital survival rate for patients with ARF with far advanced lung injury to a survival rate of 67% for patients with ARF with less severe lung injury. Low survival rates (< 20%) were seen if mechanical ventilator FIo2 was 0.80 to 1.0, while 50% of the patients with ARF survived hospitalization whose FIo2 at entry was 0.50. Peak inspiratory pressure (PIP) > 50 cm H2O at entry into the survey was associated with survival rate of less than 20%, while PIP < 30 cm H2O was associated with survival rate of 60%. Shorter periods of mechanical ventilation (< 48 h) of group A patients before entering the survey were associated with higher survival rates (38%) than patients requiring mechanical ventilation for more than 2 weeks (30%). Patients with ARF with multiorgan failure had lower survival rates (10%) than those with pulmonary dysfunction alone (45%).(ABSTRACT TRUNCATED AT 400 WORDS)

Acute Disease↗

A clinical score to predict acute renal failure after cardiac surgery.

The risk of mortality associated with acute renal failure (ARF) after open-heart surgery continues to be distressingly high. Accurate prediction of ARF provides an opportunity to develop strategies for early diagnosis and treatment. The aim of this study was to develop a clinical score to predict postoperative ARF by incorporating the effect of all of its major risk factors. A total of 33,217 patients underwent open-heart surgery at the Cleveland Clinic Foundation (1993 to 2002). The primary outcome was ARF that required dialysis. The scoring model was developed in a randomly selected test set (n = 15,838) and was validated on the remaining patients. Its predictive accuracy was compared by area under the receiver operating characteristic curve. The score ranges between 0 and 17 points. The ARF frequency at each score level in the validation set fell within the 95% confidence intervals (CI) of the corresponding frequency in the test set. Four risk categories of increasing severity (scores 0 to 2, 3 to 5, 6 to 8, and 9 to 13) were formed arbitrarily. The frequency of ARF across these categories in the test set ranged between 0.5 and 22.1%. The score was also valid in predicting ARF across all risk categories. The area under the receiver operating characteristic curve for the score in the test set was 0.81 (95% CI 0.78 to 0.83) and was similar to that in the validation set (0.82; 95% CI 0.80 to 0.85; P = 0.39). In conclusion, a score is valid and accurate in predicting ARF after open-heart surgery; along with increasing its clinical utility, the score can help in planning future clinical trials of ARF.

Acute Kidney Injury↗

Acute renal failure after bilateral nephrectomy is associated with cytokine-mediated pulmonary injury.

Clinical studies demonstrate that acute renal failure (ARF) is associated with increased mortality, which may be due to pulmonary complications. ARF may affect the lung via increased renal production or impaired clearance of mediators of lung injury, such as proinflammatory cytokines. Bilateral nephrectomy is a method to examine directly the deleterious systemic effects of absent renal clearance in ARF without the confounding effects that are associated with ischemia-reperfusion injury (e.g., ischemic ARF) or systemic toxicity (e.g., cisplatin-induced ARF). This study contrasts the effects of ischemic ARF and bilateral nephrectomy on serum cytokines and lung injury. It demonstrates that the acute absence of kidney function after both ischemic ARF and bilateral nephrectomy is associated with an increase in multiple serum cytokines, including IL-6 and IL-1beta, and that the cytokine profiles were distinct. Lung injury after ischemic ARF and bilateral nephrectomy was similar and was characterized by pulmonary vascular congestion and neutrophil infiltration. For investigation of the role of proinflammatory cytokines in pulmonary injury after ARF, the anti-inflammatory cytokine IL-10 was administered before bilateral nephrectomy. IL-10 treatment improved pulmonary architecture and was associated with a reduction in inflammatory markers, including bronchoalveolar lavage fluid total protein, pulmonary myeloperoxidase activity (a biochemical marker of neutrophils), and the chemokine macrophage inflammatory protein 2. These data demonstrate for the first time that the acute absence of kidney function results in pulmonary injury independent of renal ischemia and highlight the critical role of the kidney in the maintenance of serum cytokine balance and pulmonary homeostasis.

Acute Kidney Injury↗

Renal involvement in the systemic inflammatory reaction syndrome.

Uncontrolled infection quite often leads to systemic inflammatory reaction syndrome (SIRS) and multiorgan dysfunction (MOD) syndrome. Thirty-five consecutive patients (19 males) fulfilling strict diagnostic criteria for SIRS were enrolled in two multicenter prospective double-blind trials involving new therapies for SIRS. The patients were followed prospectively up to day 28 after the enrollment. In the 35 patients with SIRS, males predominated in the age group below 40 (10/12, 83%) compared to the older group (nine males out of 23, 39%). Out of 16 females presenting with SIRS, only two were below the age of 40. This distribution was statistically different than our general MICU population. The serum albumin in these patients was uniformly low, with a mean of 22.5 gm/L. The bulk of SIRS patients (22/35; 63%) went on to develop acute renal failure (ARF). Although statistically not different, skin and peritoneal infections were more common in ARF group while pulmonary infections in non-ARF group. The majority of blood-cultures grew gram-positive organisms. Resolution of SIRS occurred within first 3 days in greater number of non-ARF survivors than ARF survivors (6/9, 66.7% vs. 6/16, 37.5%). Of the 22 ARF patients, 17 showed improvement in their renal function; the five who did not, died before day 28. The overall mortality (about 32%) was similar in both groups. Patients who developed both ARF and ARDS did not survive. In conclusion. SIRS occurs mostly in elderly patients, almost always in patients with low albumin levels. Premenopausal women seem to be protected. Blood cultures isolated a gram-positive organism in the majority of cases. Improvement in serum creatinine suggests good prognosis. The mortality in ARF and non-ARF groups is similar.

APACHE↗

Safety of paracentesis in inpatients.

INTRODUCTION: Prior research has suggested that paracentesis is free from complications such as acute renal failure (ARF) providing albumin is administered. Actual safety of paracentesis > 1,000 ml was assessed at a tertiary care hospital. METHODS: 300 inpatient paracenteses performed between 12/99 and 4/04 were identified by coding records, of which 40 procedures were excluded due to lack of pre- or post-procedure lab values. Charts were reviewed for serum creatinine (Scr) before and after procedures, ascites volume, and clinical outcomes. RESULTS: 44 deaths occurred after 260 paracenteses (16.9%). Among 33 patients with ARF, 13 (39.4%) died. Only 31/227 patients without ARF (13.7%) died (p < 0.001). Serum creatinine (Scr) > 1.6 mg/dl prior to paracentesis predicted a 22.5% rate of ARF, compared to 8% for Scr < 1.0 (p = 0.002). ARF increased as volume increased (9.9%, 12.4%, and 14.9%, for volumes of < 2,300, 2,300 - 3,200, and > 3,200 ml) but this trend did not have statistical significance (p = 0.426). ARF occurred in 11/69 (15.9%) of patients receiving albumin, compared to 22/191 (11.5%) of patients who did not (p = 0.462). CONCLUSIONS: Paracentesis in inpatients has significant rates of ARF and death. Scr > 1.6 prior to paracentesis predicts an increased rate of ARF. Development of ARF is associated with an increased rate of death. No advantage was demonstrated with administration of albumin. Pre- and post-paracentesis labwork should be routine in inpatients.

Acute Kidney Injury↗

Acute renal failure in rhabdomyolysis.

Fifteen to 30% of patients develop acute renal failure (ARF) following rhabdomyolysis and rhabdomyolysis accounts for 5 to 9% of all ARF. Experimental studies revealed two critical factors that predispose to myoglobinuric ARF: hypovolemia/dehydration and aciduria. At the nephron level, three basic mechanisms underlie heme protein toxicity: renal vasoconstriction with decreased renal blood flow, intraluminal cast formation and direct heme protein-induced cytotoxicity. During the early phase of myoglobinuric ARF, hemodynamic process are mainly involved in glomerumar filtration rate decrease while tubular mechanisms occur in the late phase. Critical factors which predispose to myoglobinuric ARF in animal models--i.e. hypovolemia/dehydration and aciduria--are also encountered in human epidemiological studies. Prevention of myoglobinuric ARF rely on rapid and adequate correction of fluid deficits with saline, bicarbonates and mannitol. The choice of hemodialysis technique in the case of constituted ARF strongly depends on the site of intervention, especially in the case of rescue operation. The care of myoglobinuric ARF in intensive care unit do not differ from this of ARF from other causes.

Acute Kidney Injury↗

Peritoneal dialysis for management of pediatric acute renal failure.

BACKGROUND: While the use of continuous renal replacement therapies in the management of children with acute renal failure (ARF) has increased, the role of peritoneal dialysis (PD) in the treatment of pediatric ARF has received less attention. DESIGN: Retrospective database review of children requiring PD for ARF over a 10-year period. SETTING: Pediatric intensive care unit at a tertiary-care referral center. PATIENTS: Sixty-three children without previously known underlying renal disease who required PD for treatment of ARF. RESULTS: Causes of ARF were congestive heart failure (27), hemolytic-uremic syndrome (13), sepsis (10), nonrenal organ transplant (7), malignancy (3), and other (3). Mean duration of PD was 11 +/- 13 days. Children with ARF were younger (30 +/- 48 months vs 88 +/- 68 months old, p < 0.0001) and smaller (11.9 +/- 15.9 kg vs 28 +/- 22 kg, p < 0.0001) than children with known underlying renal disease who began PD during the same time period. Percutaneously placed PD catheters were used in 62% of children with ARF, compared to 4% of children with known renal disease (p < 0.0001). Hypotension was common in patients with ARF (46%), which correlated with a high frequency of vasopressor use (78%) at the time of initiation of PD. Complications of PD occurred in 25% of patients, the most common being catheter malfunction. Recovery of renal function occurred in 38% of patients; patient survival was 51%. CONCLUSIONS: Peritoneal dialysis remains an appropriate therapy for pediatric ARF from many causes, even in severely ill children requiring vasopressor support. Such children can be cared for without the use of more expensive and technology-dependent forms of renal replacement therapies.

Acute Kidney Injury↗

[Laboratory tests in acute renal failure].

This review is focused on the roles of laboratory test in acute renal failure (ARF). The roles of the laboratory test changes along with the alterations in clinical features and with the advances of treatment. Recent acute renal failure is characterized by the following three features: most of the ARF develops in hospitals, the frequency of nonoliguric ARF is increasing, and the association of other organ failure such as heart failure, liver failure or respiratory failure, increases the mortality rate. Hemodialysis is instituted in the early phase of ARF to enable the supply of enough nutriments and drugs. These features of recent ARF increases the importance of the frequent analysis of plasma creatinine in patients, who are at risk for ARF, to diagnose ARF at the onset. After the development of ARF, laboratory tests for the evaluation of other organ function is repeated. The development of new drugs increases the incidence of interstitial nephritis, and the advances in the therapeutic approach on systemic diseases (such as SLE or PN), which frequently develop ARF, alter the prognosis of these diseases. Since the early diagnosis of these diseases is important, it is necessary to develop noninvasive and reliable tests for the diagnosis of these diseases.

Acute Kidney Injury↗

[Endothelin and acute renal failure: study on their relation and possible mechanisms].

In order to investigate the role of endothelin in the pathogenesis of ARF, we determined the plasma endothelin (pET) level in different clinical ARF patients and experimental ARF rat models. It was found that pET level was significantly higher in hepatic renal syndrome (n = 9, pET 210.1 +/- 32.0 pg/ml), epidemic hemorrhagic fever (n = 18, 113.3 +/- 14.86 pg/ml), septic shock ARF (n = 8, 121.5 +/- 13.5 pg/ml), gentamicin ARF (n = 7, 55.9 +/- 6.23 pg/ml) patients, and in HgCl2 ARF (n = 8, 31.75 +/- 3.07 pg/ml), glycerine ARF (n = 8, 44.75 +/- 9.8 pg/ml) rats, compared with that of normal persons (n = 9, 33.6 +/- 3.08 pg/ml) or of normal rats (n = 10, 11.4 +/- 0.98 pg/ml). Both in the patients and animal groups, there were a linear relationship between the levels of pET and Scr (r = 0.603 4 and 0.844, P less than 0.01, respectively). Intrarenal infusion ET in dosage of 0.16 micrograms.kg-1/h produced a severe reduction of RPF and GFR in the infused kidney, without significant similar changes on the contralateral kidney. Pretreated with captopril ameliorated the renal hemodynamic changes induced by iv ET (0.67 micrograms.kg-1/h), whereas indomethacin potentiated this effect. It is concluded that both circulating or local generated ET during the ARF play an important role in the pathogenesis of ARF. RAS and PG might involve in its mechanisms.

Acute Kidney Injury↗

[Effects of free oxygen radical and nitric oxide in multiple organ dysfunction syndrome induced by acute renal failure].

OBJECTIVE: To observe the changes in free oxygen radical and nitric oxide (NO) in the liver, lung, and heart homogenate in rabbits with acute renal failure (ARF), and inquire into the mechanism of multiple organ dysfunction syndrome (MODS) subsequent to ARF. METHODS: Sixty rabbits were randomly divided into four groups (n=15 in each group). In the group I ARF was reproduced by hypodermic injection of 1% HgCl(2) in a dose of 1.3 ml/kg, and in group II ARF was reproduced by intramuscular injection of 50% glycerin in a dose of 10 ml/kg. In the control groups I and II the rabbits received an equal volume of normal saline. After 24 hours, blood samples were obtained from all the rabbits, and the liver, lung and heart were harvested and 10% homogenates were made. The blood urea nitrogen and serum creatinine were determined by automatic biochemical analyzer (Aeroset), superoxide dismutase (SOD), malondialdehyde (MDA), NO, nitric oxide synthase (NOS), and inducible nitric oxide synthase (iNOS) in tissue homogenate were also determined. RESULTS: It showed that SOD activity was significantly lowered and the MDA, NO, NOS and iNOS were significantly increased in heart homogenate of ARF groups I and II compared with control group I and II (P<0.01 or P<0.05). But these indexes in the liver and lung homogenates were not significantly different between the groups (all P>0.05). The levels of NO, NOS and iNOS in serum of ARF groups I and II were significantly increased compared with control group I and II (P<0.05 or P<0.01), and the NO contents in renal homogenate of ARF groups I and II were significantly increased compared with control group I and II (P<0.01). CONCLUSION: There is sign of damage of the myocardium in ARF, resulting in MODS. Its possible pathogenic mechanism might be attributable to free oxygen radical injury and increase in NO production. NO plays a dual role of protection and damage in the pathogenesis of ARF.

Acute Kidney Injury↗

[Study on epidemiology and etiology of hospitalized patients with acute renal failure].

OBJECTIVE: To investigate the change in epidemiology and etiology of hospitalized patients with acute renal failure (ARF) during the last years. METHODS: The data of hospitalized patients with ARF in the Third Hospital of Peking University during the last 10 years were retrospectively analyzed. The changes in epidemiology and etiology and the relative factors were studied. RESULTS: Two hundred and eleven cases from January 1994 to March 2004 were diagnosed to have ARF during the last 10 years accounting for 0.12% hospitalized patients, with an increasing trend yearly. ARF occurred in patients of all ages with two peak in the 35-45 year and 60-80 years old. The ratio of male over female was about 3 : 2. Among 211 patients, only 33 (15.6%) had renal diseases previously while 178 (84.4%) had never. Eighty-four cases (39.8%)were hospital-acquired ARF which demonstrated a significant increase after 2000 (P<0.05). One hundred and twenty-four (58.8%) were diagnosed in internal medicine with a declining trend while 87 (41.2%) were diagnosed in surgical department with a rising trend. Fifty-eight cases (27.5%) were found in intensive care unit (ICU) which demonstrated a increase by 1 89-fold after 2000.Infections, drugs and operations were the major causes for development of ARF with 61 cases (28.9%), 46 cases (21.8%) and 41 cases (19.4%) respectively. Forty-one cases (19.4%) were pre-renal, 156 cases(73.9%) were intrinsic with 72 cases (46.2%) confirmed to be ARF developed from pre-renal factors, and 14 cases (6.6%) were developed from post-renal factors. One hundred and thirty-four cases (85.9%) were acute tubulointerstitial lesions. CONCLUSION: During the last 10 years, there is an increasing trend in the incidence of ARF in hospitalized patients which might be attributed to hospital-acquired ARF due to drug, infection and operation.

Acute Kidney Injury↗