Fatal cardiac tamponade in malarial acute renal failure

Uremic hemorrhagic pericarditis occurs much less frequently in acute than in chronic renal failure, but when it does, it is a potentially fatal complication. The possibility of hemorrhagic pericarditis and cardiac tamponade should be considered in patients with acute renal failure and acute hemodynamic instability. This study reports a case of falciparum malaria complicated by acute renal failure that developed fatal cardiac tamponade in the recovery phase of acute renal failure.     

'Low-dose' dopamine worsens renal perfusion in patients with acute renal failure

'Low-dose' dopamine is frequently used in intensive care units (ICU) for its presumed renoprotective effects, but prospective and retrospective studies have so far not proven prevention or amelioration of renal injury. Data on renal perfusion following dopamine infusion are limited. In order to circumvent the problem of patient heterogeneity in the ICU setting, we used a crossover design in a prospective, double-blind randomized controlled study to investigate the effect of 'low-dose' dopamine on renal resistance indices, as determined by Doppler ultrasound. Forty patients, 10 without and 30 with acute renal failure (ARF, defined as doubling of baseline creatinine or an increase above 2 mg/dl), were included. Dopamine (2 mug/kg min) or placebo was given intravenously in alternating sequence for four subsequent periods of 60 min, starting randomly with either dopamine or placebo. Resistive (RI) and pulsatility index (PI) were closely correlated, positively related to serum creatinine values at baseline and highly reproducible during the two paired infusion periods. Dopamine reduced renal vascular resistance in patients without ARF (median RI/PI from 0.70 to 0.65/1.20 to 1.07, P<0.01) but increased resistance indices in patients with ARF (median RI/PI from 0.77 to 0.81/1.64 to 1.79, P<0.01) in the absence of effects on systemic hemodynamics. Subgroup analysis of patients with ARF revealed that dopamine induced renal vasoconstriction above 55 years (n=22) and in patients not receiving norepinephrine (n=20). In conclusion 'low-dose' dopamine can worsen renal perfusion in patients with ARF, which adds to the rationale for abandoning the routine use of 'low-dose' dopamine in critically ill patients.     

Leptospiral acute renal failure: effects of dopamine and furosemide

From unpublished experience of clinicians in the rural tropics, the combination of furosemide and dopamine is beneficial in the management of mild acute renal failure in tropical disease. We studied two groups of patients with leptospirosis and mild acute renal failure whose serum creatinine ranged from 2.4 to 5 mg/dL and fractional excretion of sodium varied from 1.21 to 2.08%. Group 1, consisting of 9 patients with the serum creatinine ranging from 2.4 to 5 mg/dL, served as the control. They received only penicillin G sodium and supportive treatment. Group 2, consisting of 8 patients with the serum creatinine ranging from 2.8 to 5 mg/dL, received, in addition to penicillin, dopamine (renal dose) and furosemide along with fluid and electrolyte replacement. The control group ran the usual clinical course of acute renal failure, and 3 patients required dialysis. There was profuse diuresis, and the recovery of renal function was faster in group 2 patients. Dopamine and furosemide are therefore useful in mild acute renal failure in leptospirosis. It is felt that this combination could be beneficial in the management of mild acute ischemic renal failure due to a clean single insult.     

Atrial natriuretic peptide and dopamine in established acute renal failure in the rat.

Recent studies have shown that atrial natriuretic peptide (ANP) alone or combined with dopamine (D) markedly improved renal function when given immediately after an ischemic insult. However, the potential beneficial effect of ANP or ANP-D in the established phase of acute renal failure (ARF) and the duration of this effect have not been examined. In the present study atriopeptin III (APIII) and D, sufficient to maintain mean arterial pressure between 100 and 110 mm Hg, or normal saline were given i.v. for four hours to awake Munich-Wistar rats (N = 6 each group) two days after ARF induction with intrarenal norepinephrine (NE). Renal function and morphology were then examined two days after treatment (Day 4). Serum creatinine (SCr) was similarly increased in both groups at the time of APIII-D or saline infusion (Day 2). By Day 4 SCr had decreased to the pre-ARF induction level in APIII-D-treated rats (P less than 0.005), but continued to rise in saline-treated animals (P less than 0.025). Day 4 renal blood flow and glomerular filtration rate (GFR) were higher in APIII-D-compared to the saline-treated group (9.13 +/- 1.14 vs. 4.41 +/- 2.25 ml/min and 0.787 +/- 0.066 vs. 0.370 +/- 0.185 ml/min, respectively, both P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)     

Synergism of dopamine plus furosemide in preventing acute renal failure in the dog

The protective effects of a combination of dopamine and furosemide were studied in dogs during the initial phase of acute renal failure (ARF) induced by intravenous uranyl nitrate (10 mg/kg). Fifteen minutes after injection of the nephrotoxin, and infusion of dopamine (3 micrograms/kg/min), furosemide (1 mg/kg/bolus followed by 1 mg/kg/hr), or both drugs simultaneously were given for 6 hours. Exogenous creatinine clearance was measured for 6 hours, and the intrarenal blood flow was measured with radioactive microspheres before and 3 hours after the induction of ARF. Treatment with both dopamine and furosemide produced renal vasodilatation, high urine flow rate, and attenuation of the fall in GRF seen in untreated animals. In contrast, single use of dopamine or furosemide was totally ineffective in producing renal vasodilation, a diuresis, or the maintenance of the GFR. These data indicate that dopamine plus furosemide have a synergistic effect in preventing the early pathophysiologic changes associated with ARF in this animal model. Maintenance of a high GFR correlated best with the enhancement of solute excretion and urine flow rate. Potential protective effects of dopamine plus furosemide in other models of ARF deserve careful investigation.     

Atrial natriuretic peptide and dopamine in a rat model of ischemic acute renal failure

Atrial natriuretic peptide (ANP) has been shown to reverse experimental models of ischemic acute renal failure (ARF). However, infusion of ANP has been associated with systemic hypotension making its use in clinical ARF impractical. Therefore, in this investigation, dopamine (D) was combined with intravenous (i.v.) atriopeptin III (AP III) to determine if this regimen was effective in reversing ARF while preventing systemic hypotension and maintaining renal blood flow (RBF). Four groups of Munich-Wistar rats were studied. Group 1, sham-ARF; Group 2, renal artery (RA) clamp (55 min) followed by i.v. saline; Group 3, RA clamp followed by i.v. AP III-D; and Group 4, RA clamp followed by i.v. D only. All infusions were begun after RA clamp release and continued for four hour. Mean arterial pressure in Group 3 rats given AP III-D were similar to that in Group 2, slightly less than that in Groups 1 and 4 (P less than 0.05), but consistently greater than 100 mm Hg during the four hour infusion. RBF in Group 3 was elevated above the level in Group 1 at P less than 0.05. Glomerular filtration rate (GFR), depressed by 52% in Group 2, was corrected to control (sham-ARF) levels in Group 3. In Group 4 there was a small but significant increase in GFR compared to Group 2 (P less than 0.05), but it remained less than that in sham-ARF or AP III-D treated ARF rats (P less than 0.01). Urine flow rate and urine sodium excretion rate were more than sixfold higher in Group 3 than any other group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Potential of dopamine A-1 agonists in the management of acute renal failure

Many therapeutic approaches have been undertaken both to prevent acute ischemic or nephrotoxic renal injury and, once acute renal failure (ARF) has developed, to improve renal function and reduce mortality. To date, most therapeutic studies have investigated the effects of diuretics (eg, mannitol, furosemide), vasoactive agents (calcium channel blockers, atrial natriuretic peptide), or dopamine (a nonselective dopaminergic agent [DAA]) in one or more phases of ARF. Unfortunately, studies of the use of DAA in ARF are complicated by the existence of at least two different DAA receptors (DA-1 and DA-2), and by the stimulation of alpha- and/or beta-adrenergic receptors by high doses of DAA. The undesirable side effects of high doses of dopamine and the inconclusive results using low doses (ie, "renal doses") of dopamine (a nonselective DAA) have prompted consideration of the use of more selective dopaminergic agonists for the prophylaxis and treatment of ARF. Selective DA-1 agonists exhibit many desirable renal effects that theoretically support their use for the prophylaxis and/or treatment of ARF, including decreases in renal vascular resistance accompanied by increases in renal blood flow and glomerular filtration rate, and increases in sodium excretion and urine volume. Even at high doses, some selective DA-1 agonists, such as fenoldopam, do not stimulate DA-2 receptors, or adrenergic alpha- or beta-receptors, and thus are free of unwanted side effects (eg, arrhythmias). Results of several studies in normal and hypertensive humans, and a few studies in animal models, are consistent with the notion that DA-1 agonists may be useful in preventing or treating ARF. Careful randomized prospective clinical trials of DA-1 agonists in human ARF are needed to test this hypothesis.     

Edema and acute renal failure

Acute renal failure (ARF) with overhydration and edematous state may follow Acute endocapillary proliferative glomerulonephritis and extracapillary glomerulonephritis, because of reduction of the glomerular capillary area available for filtration. But ARF may also be observed in edematous patients with minimal change nephrotic syndrome; it may require dialysis until recovery and is attributable to some of the following factors: (1) ischemic renal injury, (2) hypovolemia, (3) interstitial edema with tubular collapse, (4) redistribution of renal blood flow (RBF) from cortical to juxtaglomerular nephrons, (5) decrease of capillary filtration coefficient (Kf), (6) use of nonsteroidal antiinflammatory drugs. Congestive heart failure also leads to prerenal azotemia and edema formation secondary to salt retention. Multiple organ dysfunction syndrome (MODS) is frequently associated with ARF; but edema occurs even without ARF in septic patients with severe inflammatory response syndrome (SIRS). ARF may follow severe burns; burned patients are frequently edematous because of a rapid leak of fluid from the vascular bed into the wound; edema in undamaged areas occurs in the 'flow phase', because of a fall of oncotic pressure because of massive loss of plasma proteins into the wound. Edema must be treated with diuretics or by dialysis.     

Erythropoietin and acute renal failure

The hemopoietic growth factor erythropoietin (EPO) has been recognized to be a multifunctional cytokine that plays a key role in ischemic preconditioning in the brain and heart. The EPO receptor is expressed widely in the kidney, and we review the important findings from the use of EPO in experimental models of acute renal failure that show that EPO reduces tubular cell death and hence the dysfunction induced by ischemia reperfusion injury, and we explore how these observations may be translated into the clinical arena.     

Plasma dopamine, urinary dopamine and their metabolites in chronic renal failure.

To assess the clinical features of the dopamine (DA) metabolism in chronic renal failure patients (CRF), measurements were made of the plasma DA, norepinephrine (NE), epinephrine (EN) and their urinary metabolites in 6 healthy controls and 13 CRF patients before and after administration of oral DA (KW-3160, Kyowa Hakko Kogyo Co., Ltd.). The data obtained, including that for impaired DA metabolites in the patients with chronic renal failure, can be summarized as follows: I) Synthesis: In the plasma, the DA, NE and EN levels were not significantly different in the CRF patients as compared to those in normal controls, but the excretions of urinary free DA, NE and EN were markedly lower, and the free and conjugated DA, NE and EN levels were significantly decreased in the CRF patients after DA administration. These findings indicate that the plasma dopamine beta-hydroxylase activity is inhibited in CRF patients. II) Degradation: Increased levels of urinary free and conjugated 3,4-dihydroxy phenylacetic acid (DOPAC) and decreased levels of urinary conjugated homovanillic acid (HVA) were observed, indicating that the monoamine oxidase (MAO) activity in the plasma is possibly augmented, and the catecholamine O-methyl transferase (COMT) activity inhibited, in uremic patients. III) Excretion: The urinary excretions of free DOPAC, HVA, NE and vanillylmandelic acid (VMA) and of conjugated DA and DOPAC were significantly correlated with the creatinine clearance. These data suggest that the excretion of urinary DA and part of its metabolites may be regulated by the renal function.     

Acyclovir-induced acute renal failure

SUMMARY: Acyclovir is an effective antiviral agent in the treatment of herpes simplex and varicella-zoster viral infections. the best known side-effects of this drug are significant nephrotoxicity and neurotoxicity. We report on a diabetic patient with acute retinal necrosis who developed non-oliguric acute renal failure during the administration of high doses of intravenous acyclovir (500 mg/m² intravenous infusion every 8h). No obvious uremic symptoms or signs were noted. No obvious haematuria, proteinuria or crystalluria were noted in the urine. After discontinuing the acyclovir administration, renal function partially recovered. In this paper, we also review the mechanism of acyclovir-induced acute renal failure, and the precipitating factor of acyclovir-induced acute renal failure. Finally, we must once again emphasize the importance of hydration and routine check ups for renal function in preventing acyclovir-induced acute renal failure.     

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.