SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
This patient had severe dehydration and renal failure presumed to be extrarenal. After volume replacement, the course was not typical for simple extrarenal azotemia or acute tubular necrosis. Tubular handling of salt and water may not provide adequate criteria to evaluate the cause of reduced glomerular filtration rate.
Two patients had adrenal insufficiency with severe hyponatremia and profound central nervous system symptoms. In both adrenal insufficiency was diagnosed clinically. Neither patient had either hyperkalemia or azotemia.
In a review of the records of 81 patients with the discharge diagnosis of digitalis toxicity, I found a preponderance of very old patients, many of whom had anorexia, nausea, and prerenal azotemia. Arrhythmias were common (93%) and reflected enhanced automaticity, enhanced AV block, or both. Atrial fibrillation with complete heart block and a regular junctional rhythm should particularly elicit suspicion of digitalis toxicity. Atrial tachycardia with block is less specific and less frequent.
During a 61-month period, 1,458 pneumococcal isolates (including 87 bacteremia strains) were collected at the Albany Veterans Administration Medical Center and serotyped with the use of the typing system of the New York Department of Health Laboratories. Fifty percent of all isolates were of types in the 14-valent vaccine, while 68% were in 23-valent vaccine. Types 3, 6, 9, and 34 were the most prevalent types. Sixty-two percent of blood isolates were of types in the 14-valent vaccine, while 77% were in the 23-valent vaccine. Fifty-six percent of bacteremias were nosocomial and 44% were community acquired with a fatality rate of 41% and 18%, respectively. The fatality rate was greatest with risk factors such as asplenia and azotemia. These data support the recommendation for the use of 23-valent pneumococcal polysaccharide vaccine in high-risk patients, especially those who might acquire bacteremia in a nosocomial setting.
In four adults with idiopathic nephrotic syndrome and azotemia, percutaneous renal biopsy showed diabetic glomerulosclerosis, yet none had oral glucose tolerance tests diagnostic of diabetes mellitus or funduscopic evidence of diabetic retinopathy. Possible concomitant glomerular disease that may have produced proteinuria was excluded. Well documented cases of diabetic glomerulosclerosis without concurrent glucose intolerance are uncommon, and almost 30% of such patients have a past history of diabetes. Despite the absence of overt diabetes at onset of diabetic glomerulosclerosis, these patients warrant careful monitoring of plasma glucose levels and strict control of systemic hypertension.
A 56-year-old man had dyspnea, weight loss, hemoptysis, and a generalized bleeding diathesis. Physical examination disclosed hepatosplenomegaly, congestive heart failure, and multiple sites of bleeding. Severe anemia, thrombocytopenia, rouleaux formation, and a leukocytosis with circulating immature plasma cells were observed, along with azotemia, hyperuricemia, and marked elevation of total proteins with a monoclonal IgG kappa spike. The finding of increased serum viscosity confirmed the clinical impression of the hyperviscosity syndrome. Emergency plasma exchange produced marked improvement in the clinical manifestations of hyperviscosity syndrome. Systemic chemotherapy resulted in a partial remission of the disease, but the patient ultimately died of complications of treatment. In this review, we discuss the diagnosis and management of the hyperviscosity syndrome.
Angiotensin converting enzyme (ACE) inhibitors have become commonly used medications for hypertension and congestive heart failure. These agents are noted for their low incidence of adverse effects; but in certain cases, these effects can be life-threatening. Severe hyperkalemia is one of the potentially dangerous effects of the ACE inhibitors. While cases of life-threatening hyperkalemia associated with the use of ACE inhibitors have been described previously, in no instance was dialysis required. Herein, we report a case of acute hyperkalemia in a patient with congestive heart failure and renal insufficiency, the resolution of which required hemodialysis. The hyperkalemia in this case occurred without an increase in the patient's azotemia. In addition, the patient did not respond to attempts to effect the intracellular shift of potassium. This suggested that there may have been a defect in internal potassium homeostasis.
A 42-year-old man came to our emergency room hyperthermic (oral temperature, 42.4 degrees C), diaphoretic, and delirious. Other findings included labile blood pressure, sinus tachycardia (heart rate, 138/min), tachypnea (respiratory rate 34/min), muscle rigidity, and incontinence. Two days earlier, he had gone to a local clinic with complaints of abdominal pain, nausea, and vomiting. Promethazine was prescribed, and this was the patient's only medication on admission. Laboratory studies showed leukocytosis, hypernatremia, metabolic acidosis, elevated creatinine phosphokinase level, elevated transaminase levels, azotemia, hyperkalemia, hyperphosphatemia, hypocalcemia, and myoglobulinuria. The clinical and laboratory findings were characteristic of the neuroleptic malignant syndrome, with promethazine as the offending agent.
Canine kidneys, flushed with either Collins solution or autologous cryoprecipitated plasma, were then stored for 24 hr by either simple cold storage (submersion) in the flushing solution, or by continuous hypothermic pulsatile perfusion with cryoprecipitated plasma. After autotransplantation without contralateral nephrectomy, detailed split renal function studies were carried out immediately as well as 2 and 7 days later. Measurements were made of inulin clearance, maximal transport of p-aminohippurate, reabsorption of sodium, chloride, and glucose, and the reabsorption of free water. Contralateral nephrectomy was performed 7 days after transplantation, following measurement of renal functions on that day, and plasma urea nitrogen and creatinine were measured periodically over the ensuing 3 weeks. Renal function after transplantation was affected very little by the choice of flushing solution, and the course of azotemia that developed following contralateral nephrectomy was the same in all groups. However, the detailed functional measurements showed that during the 7-day period after transplantation, renal function was depressed to a much greater extent in kidneys treated by simple cold storage than in those that had been perfused.
Physiologic and morphologic techniques were used to study kidneys of cardiac transplant recipients treated with either low-dose (low-CsA) or high-dose (high-CsA) cyclosporine. After 12 months both low-CsA (4.6 +/- 0.4) and high-CsA (6.3 +/- 0.3 mg/Kg/24 hr, p less than 0.01) were associated with azotemia and hypertension; GFR with each regimen was depressed below values in a third group treated without CsA (no-CsA) by 40-47%, while corresponding renal vascular resistance was elevated greater than 2-fold (P less than 0.01). Morphologic changes in both CsA groups included an obliterative arteriolopathy with downstream collapse or sclerosis of glomeruli. Determination of renal arcuate vein occlusion pressure revealed an increasing renal artery-to-peritubular capillary pressure gradient between 1 and 12 months of CsA therapy. Fractional clearances of dextrans of graded size were elevated at each time compared with the no-CsA group. Analysis of dextran transport with an isoporous membrane model indicates that transglomerular hydraulic pressure difference (delta P) approximated 39 with no-CsA, but was reduced with low-CsA therapy to about 30 at 1 month, and about 34 mmHg after 12 months. We conclude that chronic CsA therapy induces constriction and eventual occlusion of afferent arterioles, causing downstream glomerular damage that is irreversible. Low versus high dosage of CsA confers only marginal protection against this serious microvascular injury.
Between January 1977 and March 1988, 10 of 892 renal transplant recipients formed urinary tract calculi posttransplantation. The presenting symptoms were predominantly those of azotemia due to obstruction and/or hematuria. Factors predisposing to stone formation included a reconstructive urologic procedure at the time of transplantation (n = 4) or a surgical complication (n = 4), necessitating the placement of a ureteral stent and/or nephrostomy tube, secondary hyperparathyroidism (n = 5), hyperuricosuria (n = 4), and hypercalciuria (n = 1). Four patients passed their stones spontaneously; 1 patient underwent ureterolithotomy, 3 patients underwent endourologic stone extraction, 1 patient was treated with a combination of surgical and endourologic procedures, and 1 patient underwent extracorporeal shock wave lithotripsy as monotherapy. While the management of these patients can be challenging, awareness of predisposing factors, proper application of all currently available urologic techniques, and attention to certain guidelines of management can aid in minimizing morbidity from this rare urologic complication of renal transplantation.
We compared the efficacy of continuous intraarterial versus intravenous 6-mercaptopurine (6-MP) infusion in a mongrel canine renal allograft model with regard to overall survival, incidence of systemic and renal toxicity, and systemic drug exposure. Arterial anastomoses were done end-to-end, and infusion catheters were placed in the iliac artery or vena cava and connected to a subcutaneously placed programmable pump. A dose of 0.5 mg/kg/day 6-MP did not prolong survival over heparin-treated or untreated controls (MST = 7 days for both groups) when administered either locally or systemically. However, 0.75 mg/kg/day 6-MP i.a. (MST = 20 days) significantly prolonged survival over both untreated (P = 0.007) and heparin-treated controls (P = 0.02), with all dogs eventually dying of rejection. In contrast, 0.75 mg/kg/day i.v. (MST = 7 days) failed to prolong survival over controls (P greater than 0.1) and produced death from systemic toxicity in 3 of 7 animals. Six of 7 dogs receiving 2.0 mg/kg/day 6-MP i.a. (MST = 12 days) developed azotemia secondary to drug-induced nephrotoxicity. Identical renal histologic changes occurred in the same time frame in autotransplants treated similarly. Of 7 animals receiving 2.0 mg/kg/day i.v. (MST = 12 days), 5 died from early, severe systemic drug toxicity and 2 from early rejection. During 6-MP infusion at 0.5 mg/kg/day, systemic exposure was significantly less in the locally treated than in the systemically treated dogs when Cr concentrations were normal or moderately elevated (P less than 0.0005 and P = 0.01, respectively) but not when renal function became severely impaired (P = 0.34). In contrast to i.v. infusion, i.a. 6-MP delivery dissociated immunosuppressive efficacy from systemic toxicity, supporting previous work demonstrating high first-pass renal elimination of 6-MP. We conclude that tightly controlled local delivery of an immunosuppressive agent can effectively prolong graft survival with reduced systemic toxicity in a large animal model employing a pump/catheter system applicable to man.
BACKGROUND: The piggyback technique of orthotopic liver transplantation is an attractive alternative that preserves the recipient inferior vena cava and allows uninterrupted venous blood return during the anhepatic phase. As with other transplantation techniques, the vascular anastomoses required by the piggyback technique can develop strictures. METHODS: Review of records of 264 piggyback transplantations revealed two cases of delayed-onset hepatic venous obstruction from anastomotic strictures. Both patients also had symptoms of inferior vena cava obstruction, with azotemia and lower extremity edema. Both patients were treated percutaneously with balloon-expandable stents. RESULTS: Rapid, dramatic resolution of symptoms was achieved in both patients. Patients remain completely asymptomatic at 39 and 3 months of follow-up. CONCLUSIONS: Hepatic venous anastomotic strictures in recipients of piggyback technique transplants are a very uncommon complication. They may be easily and effectively treated by minimally invasive endovascular intervention.
BACKGROUND: No definitive antiviral therapy exists for adenovirus (ADV) in immunosuppressed hosts. Cidofovir (CDV), a broad spectrum anti-DNA viral agent, has previously been shown to be of therapeutic benefit in life-threatening adenoviral disease in bone marrow stem-cell recipients. METHODS: A 71/2-month-old girl with a history of biliary atresia developed fevers, hematochezia, tachypnea, and laboratory evidence of hepatitis and pancreatitis 12 days after liver transplantation. A stool culture, oropharyngeal culture, blood viral culture, and blood polymerase chain reaction (PCR) confirmed ADV. Cidofovir 1 mg/kg intravenously three times per week was initiated. The patient received intravenous hydration and probenecid with the infusions to reduce the nephrotoxicity of CDV. Immunosuppression was reduced to achieve tacrolimus trough levels of approximately 8 ng/mL and prednisone at 0.1 mg/kg per day. Complete blood cell count, urinalysis, and viral studies were obtained weekly. RESULTS: Detection of ADV DNA by PCR made a transition from positive to negative during CDV therapy. Blood viral cultures became negative after two CDV doses. Alanine aminotransferase normalized by 5 weeks of therapy. CDV was discontinued after 7 weeks secondary to transient acidosis and proteinuria. The patient never developed azotemia, neutropenia, or ocular abnormalities. CONCLUSIONS: CDV was associated with improved clinical status, viral clearance, and minimal transient side effects in a pediatric liver transplant recipient with disseminated adenoviral disease. The current report documents clearance of disseminated ADV infection in a liver transplant recipient receiving CDV infusions.
Abdominal sepsis and septic shock are still major causes of mortality in intensive care units (ICU). Acute renal failure (ARF) is one of the hallmarks encountered in septic shock. The pathophysiological alterations leading to ARF are poorly understood. A novel murine model of polymicrobial sepsis (colon ascendens stent peritonitis [CASP]) was used to investigate functional renal parameters, renal chemokine transcription levels, and recruitment of inflammatory leukocytes in septic ARF. CASP was induced by inserting a 14-gauge stent into the colon ascendens of C57BL/6 mice, generating a septic focus resulting in polymicrobial sepsis. Mice were monitored for urine output and serum azotemia. Kidneys were harvested for analysis of leukocyte infiltration by immunohistochemistry and chemokine gene expression by RNase protection assay (3, 6, 12, and 18 h). CASP, but not sham-CASP, resulted in anuria immediately after surgery and in elevated serum creatinine and BUN detected 18 h after CASP surgery, confirming acute renal failure. Progressive induction of chemokine gene expression was observed for IP-10, MIP-2, MIP-1alpha, MIP-1beta, MCP-1, and RANTES peaking at 12 h with subsequent decrease. Immunohistochemistry revealed an accumulation of neutrophils and monocytes which had adhered to the renal vascular endothelium. Thus, acute renal failure in sepsis is accompanied by a marked upregulation of chemokines of the CC and CXC group within the kidney.
Angiotensin-converting enzyme inhibitors (ACEIs) are contraindicated in patients with bilateral renal artery stenosis due to risk of azotemia resulting from preferential efferent arteriolar vasodilation in the renal glomerulus due to inhibition of angiotensin II. Patients with renal artery stenosis who can derive survival benefit from ACE inhibition, therefore, may not receive ACEI therapy. We evaluated the safety of ACEI therapy in patients with bilateral renal artery stenosis following successful revascularization using renal artery stenting. This study is a retrospective analysis of 25 patients who underwent bilateral renal artery stenting for refractory hypertension and had a strong clinical indication for long-term ACEI use (left ventricular dysfunction or diabetes). Eighteen of the 25 patients (72%) have been safely maintained on a target dose of ACEIs, 2 of the 25 have been treated with angiotensin receptor blockers due to cough, and 5 of the 25 are being treated with a hydralazine/nitrate combination due to cough (2 patients) or baseline renal insufficiency (3 patients). We conclude that patients with bilateral renal artery stenoses that have been successfully revascularized using renal stenting may be safely treated with long-term ACEI therapy.
The evaluation and management of acute renal failure in the ICU patient remains a formidable task because of the complexity of this condition. Clinical and physiologic assessment and complementing laboratory and imaging tests are currently insufficient to differ between true renal parenchymal damage (acute tubular necrosis; it is important to realize that this term does not necessarily imply widespread injury, because whole organ dysfunction in humans has often been associated with very limited parenchymal cellular necrosis) and prerenal azotemia (decreased renal blood flow with altered glomerular hemodynamics and subsequently diminished glomerular filtration, without significant epithelial cell injury). Moreover, tubular damage and altered glomerular hemodynamics may coexist or lead to each other, and their relative contribution to the evolving renal dysfunction has not been unequivocally established. The limited data regarding the renal pathology of such patients and the scant information about human morphologic and functional correlates further undermine our knowledge about diagnostic and therapeutic approaches to these patients. Advanced techniques are critically needed to establish noninvasively the dynamic status of renal parenchymal microcirculation and the distribution of intrarenal oxygenation and to identify evolving cellular energy depletion and tubular cell damage. A few technologies are potentially promising, such as blood oxygen level dependent magnetic resonance imaging, positron emission tomography, and kidney injury molecule-1 detection in patients' urine. Because of the difficulties in analyzing the pathophysiology in humans, clinicians continue to rely largely on animal models to guide understanding and rationale for the identification of therapeutic targets. Data from such animal studies are complemented by studies in isolated perfused kidneys, isolated tubules, and tubular epithelial cell cultures. In this report, we summarize some concepts of acute tubular necrosis that have evolved as a result of these studies, evaluate available animal models, and underscore controversies regarding experimental acute tubular necrosis.
Acute renal failure results in significant morbidity and mortality, yet renal failure is not the usual cause of death in the clinical situation. We have previously reported systemic increases in the inflammatory mediators tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1) after renal ischemia in the mouse. In the present study, an animal model of bilateral renal ischemia was used to test the hypothesis that cytokines released with renal ischemia have effects on other organ systems. Increased levels of immunoreactive TNF-alpha and IL-1 and intercellular adhesion molecule-1 mRNA were found in the heart after renal ischemia in the rat. This was accompanied by increases in myeloperoxidase activity, an index of tissue leukocyte infiltration, in the heart as well as the liver and lung. Functional changes in the heart 48 h after renal ischemia included increases in left ventricular end diastolic diameter, left ventricular end systolic diameter, and decreased fractional shortening by echocardiography. Evidence of apoptosis of cardiac cells was also found 48 h after an abbreviated period of renal ischemia insufficient to induce azotemia but not bilateral nephrectomy (which resulted in significant renal failure), suggesting that renal ischemia but not uremia is necessary for the apoptosis observed. It was also found that blocking the action of TNF-alpha limited cardiac apoptosis. Renal ischemia results in distant effects and the alterations observed in the heart may be important in the morbidity and mortality observed clinically.