Resolution Of Acute Renal Failure Research Articles

Bilateral Renal Infiltration by Burkitt Lymphoma: Case Report

Non-Hodgkin lymphomas represent the third leading cause of cancer in the pediatric age group. Primary renal lymphoma is an uncommon presentation. We describe the diagnosis and treatment of a 6-year-old boy who presented with bilateral renal involvement, abdominal pain, vomiting, and weight loss. Initial investigations were consistent with presumed non-oliguric end-stage renal disease and anemia. Subsequent imaging demonstrated enlarged kidneys bilaterally. Histology revealed a Burkitt lymphoma that was highly responsive to chemotherapy, including the anti-CD20 monoclonal agent rituximab. Specific treatment was introduced with corticosteroids, vincristine, cyclophosphamide, and rituximab, resulting in the resolution of acute renal failure within 72 hours and complete response at the second induction with ANHL 1131 protocol.

Telaprevir in a Patient with Chronic Hepatitis C and Cryoglobulinemic Glomerulonephritis

Mixed cryoglobulinemia (MC), the most common extrahepatic manifestation of HCV, may lead to renal involvement ranging from mild urinary abnormalities to nephritic syndrome, eventually evolving to renal failure requiring renal replacement therapy. HCV eradication with pegylated interferon (PEG-IFN) and ribavirin (RBV) is the only curative treatment for MC-related membranoproliferative glomerulonephritis. The addition of directly acting antivirals (DAAs) to PEG-IFN and RBV has significantly improved sustained virological response rates in HCV genotype 1 patients. Safety and efficacy of this regimen in patients with membranoproliferative glomerulonephritis has not been proved yet. Here, we report the case of a woman with HCV-1-related cryoglobulinemic membranoproliferative glomerulonephritis presenting with severe nephritic syndrome and rapidly progressive renal failure, who received successful treatment with the DAA telaprevir in conjunction with PEG-IFN and RBV. Triple therapy was safe and effective, leading to HCV eradication and complete resolution of acute renal failure.

Low-Dose Aminophylline for the Treatment of Neonatal Non-Oliguric Renal Failure—Case Series and Review of the Literature

Aminophylline is a methylxanthine with multiple physiologic actions. At low doses, aminophylline can antagonize adenosine and improve renal function via increased glomerular filtration rate. Despite its clinical use, little data exists in neonates for this indication. Therefore, the objective of this report is to describe the impact of aminophylline on renal function indices in a series of neonates with acute renal failure. This was a retrospective chart review of 13 neonates with acute renal failure who received aminophylline during a 15-month study period. Aminophylline was administered at 1 mg/kg intravenously or orally every twelve hours. Forty-six percent (n = 6) of the patients received a 5 mg/kg loading dose before initiation of maintenance therapy. Most patients had already received other treatments for renal failure, including diuretics and dopamine. Resolution of acute renal failure (with normalization of serum creatinine and blood urea nitrogen) was documented in 10 patients (77%). Four of the thirteen patients died from complications due to their prematurity. Failure of low-dose aminophylline was observed in 3 of the 4 patients who died. Low-dose aminophylline in neonates with acute renal failure is associated with an improvement in renal function indices.

Index of suspicion in the nursery

A set of nonidentical twins is born at 24 weeks gestational age by normal spontaneous vaginal delivery to a 25-year-old gravida 3 para 2 female. The infants are appropriate for gestational age, weighing 525 and 520 g. Both twins are intubated in the delivery room, given surfactant via endotracheal tubes, and placed on high-frequency oscillators in the neonatal intensive care unit (NICU). Results of clinical examination on admission to the NICU are normal for both twins. On the fourth day after birth, each infant is started on continuous fentanyl infusions at 3 mcg/kg per hour. Urinary output begins to decline 24 hours after initiation of the fentanyl infusions, with a simultaneous decline in renal function (TableT1). On postnatal day 7, marked abdominal distention is noted in both twins.Renal ultrasonography on both infants reveals bilateral hydronephrosis and very distended, urine-filled bladders extending under the hepatic border (Figs. 1 and 2). Fentanyl infusions are discontinued, and indwelling catheters are inserted, allowing bladder drainage in each infant. After catheterization, both twins experience polyuria and improvement in renal function. Repeat renal ultrasonography on postnatal day 9 demonstrates resolution of hydronephrosis and normal bladder size (Figs. 3 and 4)The association between fentanyl infusion and bladder urinary retention remains unknown. The first step in elucidation begins with the differential diagnosis of urinary tract obstruction and hydronephrosis in neonates. The clinician must rule out transient in utero hydronephrosis, tumors, urologic anomalies, and bladder asphyxia. Renal ultrasonography can be performed to rule out ascites or renal vascular diseases as the cause for acute renal failure. The next step involves understanding the mechanism of bladder retention with fentanyl use.There are numerous possible mechanisms for fentanyl-induced bladder retention. The causative mechanism is relaxation of the detrusor muscle and increased urinary bladder compliance. Mechanisms that have been gleaned from animal studies indicate that morphine and other opiates cause urinary retention by activating mu- and delta-opioid receptors in the spinal cord and midbrain periaqueductal gray (PAG) region. Terris and Merguerian found urinary retention to be induced by an increase in urethral sphincter pressures.These infants presented with deteriorating renal function and acute urinary retention requiring urethral catheter placement. Each patient’s prenatal ultrasonography image was normal, which ruled out posterior uretheral valves. Each patient had normal urine output and displayed normal renal function prior to starting fentanyl infusions. The absence of bladder trabeculation signifies a lack of long-standing outflow obstruction. In these twin infants, infusions of fentanyl resulted in bladder outflow obstruction and bilateral ureteral obstruction. The insertion of indwelling catheters allowed drainage of 30 and 25 mL of urine from each bladder. Cessation of the fentanyl infusions resulted in resolution of acute renal failure and hydronephrosis. Follow-up renal ultrasonography showed resolution of urinary bladder distention and hydronephrosis, which strongly suggests that fentanyl infusions were associated with the bladder obstructions.Utpala and associates reported two cases of preterm infants (unrelated) who had urinary retention and renal failure due to continuous fentanyl infusions, both of whom had mild swelling of the suprapubic area. In the twins in this case, marked bladder distention extended beyond the hepatic border.After confirmation of urinary retention through physical examination and renal ultrasonography, discontinuing the causative agent and helping the body eliminate excess fluid should prove beneficial in reversing urine retention. Discontinuing fentanyl should reverse the process causing the urine retention, and catheter placement provides a conduit for fluid to escape from the bladder.Long-term complications with continued use of fentanyl infusions after the development of anuria remain largely undefined, but they may involve organ damage, loss of function, or the need for transplantation.Neonatal urinary obstruction is rare, but must be considered in infants who are receiving fentanyl infusions. Infants may present with decreased urine output and abdominal distention after initiation of such infusions. Discontinuing fentanyl infusions and inserting indwelling urinary catheters proved beneficial in evacuating the bladders and improving renal function in this case.

Salvage stenting for acute renal failure secondary to renal artery stenosis

We present two cases of successful, emergency renal artery stenting in the setting of acute renal failure requiring dialysis secondary to renal artery stenosis. Early reopening of the stenotic renal artery led to the resolution of acute renal failure and obviated the need for further dialysis in both cases.

Acute renal failure secondary to spontaneous acute tumor lysis syndrome in myelofibrosis

A 70-year-old man with myelofibrosis developed nonoliguric acute renal failure in association with acute uric acid nephropathy in the absence of chemotherapy or radiotherapy. The patient had an 18-month history of transfusion-dependent myelofibrosis and moderate chronic renal insufficiency. Admission laboratory findings were remarkable for severe hyperuricemia, hyperphosphatemia, hyperkalemia, and hypocalcemia with acute deterioration of renal function, consistent with a diagnosis of acute uric acid nephropathy. Treatment, including hemodialysis and allopurinol administration, resulted in clinical improvement with normalization of serum uric acid concentrations and resolution of acute renal failure. With long-term allopurinol therapy, renal function has remained at his previous baseline, and there has been no transformation to acute leukemia. This case represents a rare instance of acute renal failure related to the occurrence of acute uric acid nephropathy associated with myelofibrosis and emphasizes the importance of early recognition and aggressive management, which can lead to recovery of renal function. © 2001 by the National Kidney Foundation, Inc.

Long-term follow-up of acute renal failure caused by angiotensin converting enzyme inhibitors

Angiotensin converting enzyme (ACE) inhibitors are useful in the treatment of hypertension and heart failure. However, acute renal failure (ARF) may occur in patients who are taking these drugs in situations associated with decreased glomerular filtration pressure, such as dehydration caused by acute diarrhea or diuretic therapy. Sixty-four patients who were admitted to the intensive care unit for ARF associated with ACE inhibitor therapy were followed for more than 5 years. In this historical retrospective study, we documented that 45 patients were treated for hypertension (group I) and 19 were treated for heart failure (group II). Their mean age was 71.2 ± 11.6 years. Patients with ARF presented with overt dehydration in 91% and 84% of the cases in groups I and II, respectively. Hypovolemia was caused by diuretics or gastrointestinal fluid loss. Bilateral artery-renal stenosis or stenosis in a solitary kidney was documented in 22% and 10% of patients in groups I and II, respectively. The probability of survival was 91% and 49% at 1 year and 64% and 18% at 5 years, for groups I and II, respectively. Acute renal failure required hemodialysis in seven patients, but none of them became dialysis dependent. In the subgroup of patients with preexisting chronic renal failure, all the patients except for one who belonged to group II died within 2 years. In both groups, after resolution of ARF, plasma creatinine concentration returned to baseline level and the course of renal function was not significantly worsened. In conclusion, ARF associated with ACE inhibitors is likely to occur in many patients without renal artery stenosis after unexpected dehydration, especially in older patients with congestive heart failure. In both groups of patients, in the absence of preexisting chronic uremia, recovery of renal function occurred without sequelae, even after an episode of acute tubular necrosis requiring dialysis.

Gastrointestinal Manifestations of Hemolytic Uremic Syndrome

A retrospective study of 76 children with hemolytic uremic syndrome (HUS) who were admitted to the Alberta Children's Hospital in Calgary. Alberta between January 1982 and December 1988 was undertaken to explore the gastrointestinal manifestations of the syndrome. The children (mean age of 4.0 +/- 3.1 years) presented primarily during the summer months with a microangiopathic hemolytic anemia (Hgb 94 +/- 26 g/L), thrombocytopenia (platelets 87 +/- 83 X 10(9)/L), and acute renal failure (oligoanuria with a BUN of 26 +/- 15 mmol/L, and a creatinine of 294 +/- 90 mumol/L). Forty-three children required dialysis for 10 +/- 17 days. The duration of hospitalization was 17 +/- 17 days. Four children died of complications attributable to HUS. The following symptoms and gastrointestinal manifestations of HUS were noted: fever (33%), vomiting (80%), abdominal discomfort/tenderness (59%), diarrhea (100%), hemorrhagic colitis (79%), rectal prolapse (13%), colonic stricture (3%), colonic perforation (1%), intussusception (1%), indirect hyperbilirubinemia (49%), and elevated hepatocellular enzymes (58%). Of the last 29 children studied, 19 (66%) had elevated levels of amylase and lipase in the presence of acute renal failure, and six (21%) had a marked elevation of lipase (more than four times normal) with additional supportive evidence of pancreatitis. The additional supportive evidence included persistent elevation of lipase after the resolution of acute renal failure in four children, a marked increment in lipase in association with abdominal pain and an abnormal ultrasound of the pancreas after the initiation of oral feeding in a fifth child, and pancreatic exocrine and endocrine necrosis at autopsy in a sixth child.(ABSTRACT TRUNCATED AT 250 WORDS)

Gastrointestinal Manifestations of Hemolytic Uremic Syndrome

A restrospective study of 76 children with hemolytic uremic syndrome (HUS) who were admitted to the Alberta Children's Hospital in Calgary, Alberta between January 1982 and December 1988 was undertaken to explore the gastrointestinal manifestations of the syndrome. The children (mean age of 4.0 ± 3.1 years) presented primarily during the summer months with a microangiopathic hemolytic anemia (Hgb 94 ± 26 g/L), thrombocytopenia (platelets 87 ± 83 x 109/L), and acute renal failure (oligoanuria with a BUN of 26 ± 15 mmol/L, and a creatinine of 294 ± 90 μmol/L). Forty‐three children required dialysis for 10 ± 17 days. The duration of hospitalization was 17 ± 17 days. Four children died of complications attributable to HUS. The following symptoms and gastrointestinal manifestations of HUS were noted: fever (33%), vomiting (80%), abdominal discomfort/tenderness (59%), diarrhea (100%), hemorrhagic colitis (79%), rectal prolapse (13%), colonic stricture (3%), colonic perforation (1%), intussusception (1%), indirect hyperbilirubinemia (49%), and elevated hepatocellular enzymes (58%). Of the last 29 children studied, 19(66%) had elevated levels of amylase and lipase in the presence of acute renal failure, and six (21%) had a marked elevation of lipase (more than four times normal) with additional supportive evidence of pancreatitis. The additional supportive evidence included persistent elevation of lipase after the resolution of acute renal failure in four children, a marked increment in lipase in association with abdominal pain and an abnormal ultrasound of the pancreas after the initiation of oral feeding in a fifth child, and pancreatic exocrine and endocrine necrosis at autopsy in a sixth child. This study reviews the gastrointestinal manifestations of HUS in a large series of patients and presents data to suggest that pancreatitis is a relatively common complication of HUS.

Resolution of Acute Renal Failure in Toxoplasmic Encephalitis Despite Continuance of Sulfadiazine

A patient with AIDS and toxoplasmic encephalitis treated with pyrimethamine and sulfadiazine became hypovolemic and developed acute renal failure. Diagnostic sulfadiazine crystals were abundant in the urine, and ultrasound examination demonstrated sludge and stones, presumably due to sulfadiazine. Renal failure resolved rapidly with hydration and administration of alkali, despite continued administration of sulfadiazine. The relatively old literature concerning crystalluria and renal failure due to sulfonamides is reviewed briefly, since complications due to use of poorly soluble sulfonamides probably will become more widespread as toxoplasmic encephalitis becomes more prevalent.

Postoperative Enhancement of Urinary Output in Patients with Acute Renal Failure Using Continuous Furosemide Therapy

Three cardiac surgical patients with acute postoperative renal failure were treated with a constant infusion of furosemide (Lasix) after furosemide given in bolus proved ineffective. Furosemide given continuously brought about a prompt resolution of the oliguria and tended to hasten the resolution of acute renal failure.