Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two brothers, 29 and 33 years of age, had recurrent myoglobinuria, renal failure and azotemia, but were otherwise normal, without apparent muscle weakness or exercise intolerance. Ischemic exercise resulted in normal lactate production. Muscle glycogen content and activities of phosphorylase and phosphofructokinase were normal. Plasma triglycerides were elevated (500 mg per deciliter) on a regular diet and rose during fasting. During a 72-hour fast, serum creatine phosphokinase rose more than 10 times, and myoglobin was detected in urine. Plasma ketone production was minimal during fasting, but prompt ketonemia ( a normal response) occurred after ingestion of medium-chain triglycerides. Carnitine palmityl transferase activity was virtually absent in crude muscle extracts and mitochondrial fractions. Lack of this enzyme impairs long-chain fatty acid utilization, reflected in increased content of plasma free fatty acids and plasma triglycerides. Depletion of ATP because of this metabolic block in muscle may account for the attacks of myoglobinuria.
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PMID:A disorder of muscle lipid metabolism and myoglobinuria. Absence of carnitine palmityl transferase. 12 38

Eight sailors on board the Asiafreighter were exposed to arsine that had escaped from a cylinder in the cargo hold. Four suffered severe toxicity and within a few hours had developed fever, weakness, nausea, vomiting, diarrhoea, abdominal pain, and haemoglobinuria. These patients had pronounced intravascular haemolysis, which in one patient was complete. This patient was also stuporose and anoxic, a condition attributed to failure of oxygen transport and sludging of red cell debris in the cerebral and pulmonary circulations, but he regained a normal level of consciousness after exchange transfusion. Evidence of marrow depression was present: the reticulocyte response to the haemolysis was poor and there was a thrombocytopenia. All four patients developed renal failure, one being totally anuric for five weeks. Two patients developed peripheral neuropathy, and one was still severely disabled six months after the incident. The other four patients had a similar, though less severe, illness.
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PMID:Arsine toxicity aboard the Asiafreighter. 16 42

A 54-year-old woman had muscle disease that terminated fatally with complete body paralysis. The patient had renal failure, which progressed concurrently with her muscle weakness. Myoglobinuria was not demonstrated during the active stage of her illness. Renal biopsy specimens demonstrated immune deposits in the glomeruli, and, at autopsy, there was a generalized glomerulonephritis. We believe the muscle disease was a consequence of acute rhabdomyolysis, hyperacute polymyositis, or virus infection. Regardless of the nature of the muscle disease, an immune mechanism may have been responsible for the associated renal failure.
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PMID:Muscle disease associated with renal failure. 30 32

A 35-year-old patient with terminal renal failure who had received 30 mg piperazine hexahydrate/kg body weight daily for 10 days for oxyuriasis was subsequently admitted to hospital in precoma with severe clinical symptoms not unlike those observed in so-called dialysis dementia: loss of consciousness, dysarthria, apraxia, clonic spasms, tremor, muscular weakness, dropping of objects, inability to think clearly and/or hallucinations. The EEG showed disturbances with diffuse, multifocal delta waves. Under maintenance hemodialysis the patient became asymptomatic one week after discontinuation of the piperazine therapy. Piperazine is contraindicated in patients with renal failure.
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PMID:[Piperazine intoxication in long-term hemodialysis]. 41 54

Drugs that are administered to man may be biotransformed to yield metabolites that are pharmacologically active. The therapeutic and toxic activities of drug metabolites and the species in which this activity was demonstrated are compiled for the metabolites of 58 drugs. The metabolite to parent drug ratio in the plasma of non-uraemic man and the percentage urinary excretion of the metabolite in non-uraemic man are also tabulated. Those active metabolites with significant pharmacological activity and high plasma levels, both relative to that of the parent drug, will probably contribute substantially to the pharmacological effect ascribed to the parent drug. Active metabolites may accumulate in patients with end stage renal disease if renal excretion is a major elimination pathway for the metabolite. This is true even if the active metabolite is a minor metabolite of the parent drug, as long as the minor metabolite is not further biotransformed and is mainly excreted in the urine. Minor metabolite accumulation may also occur if it is further biotransformed by a pathway inhibited in uraemia. Some clinical examples of the accumulation of active drug metabolites in patients with renal failure are: (a) The abolition of premature ventricular contractions and prevention of paroxysmal atrial tachycardia in some cardiac patients with poor renal function treated with procainamide are associated with high levels of N-acetylprocainamide. (b) The severe irritability and twitching seen in a uraemic patient treated with pethidine (meperidine) are associated with high levels of norpethidine. (c) The severe muscle weakness and tenderness seen in patients with renal failure receiving clofibrate are associated with excessive accumulation of the free acid metabolite of clofibrate. (d) Patients with severe renal insufficiency taking allopurinol appear to experience a higher incidence of side reactions, possibly due to the accumulation of oxipurinol. (e) Accumulation of free and acetylated sulphonamides in patients with renal failure is associated with an increase in toxic side-effects (severe nausea and vomiting, evanescent macular rash). (f) Peripheral neuritis seen after nitrofurantoin therapy in patients with impaired renal function is thought to be due to accumulation of a toxic metabolite. The high incidence of adverse drug reactions seen in patients with renal failure may for some drugs be explained in part, as the above examples illustrate, by the accumulation of active drug metabolites. Monitoring plasma levels of drugs can be an important guide to therapy. However, if a drug has an active metabolite, determination of parent drug alone may cause misleading interpretations of blood level measurements. The plasma level of the active metabolite should also be determined and its time-action characteristics taken into account in any clinical decisions based on drug level monitoring.
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PMID:Pharmacologically active drug metabolites: therapeutic and toxic activities, plasma and urine data in man, accumulation in renal failure. 79 49

Adverse effects occurred in four youths after intravenous injection of an aqueous cannabis-seed tea, which was prepared by boiling the seeds. The effects were immediate and included nausea, vomiting, abdominal pain, watery diarrhea, chills, fever, hypovolemic shock, hypotension, and non-oligemic transitory renal failure. Other manifestations included persistent hypoglycemia, tachycardia, gastrointestinal bleeding, conjunctival hemorrhage, injury, jaundice, splenomegaly, leucocytosis, myalgia, arthralgia, motor weakness, and prostration. Ischemia was noted on electrocardiogram (EKG). All manifestations appeared to reverse within weeks, but these effects had been potentially fatal.
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PMID:Adverse effects of intravenous cannabis tea. 87 75

31 adult patients (15 male and 16 female) with chronic renal failure were treated for 6 months with 1-alfa-hydroxycholecalciferol on a dose 0.25-2.0 micrograms/24 h. 15 patients with not very advanced renal failure (serum creatinine level 176.8-442 mumol/l) received conservative therapy (group I), 16 patients with serum creatinine value 884-1326 mumol/l were treated by intermittent hemodialysis (group II). The statistically significant decrease of serum alkaline phosphatase activity in group I and II (p < 0.01), the rise of serum calcium level in group I (p < 0.005) were determined. Half of the patients from both the groups stated the relief or disappearance of bone and joint pains and muscle weakness. Besides in group I significant decrease of creatinine clearance (p < 0.001) and increase of serum urea and creatinine value (p < 0.01) were noticed. On the basis of these results we can conclude that the treatment with 1-alfa-hydroxycholecalciferol, produced by "Polfa", ought to be introduced gradually with increasing doses and frequent monitoring of calcium-phosphate metabolism and renal function parameters.
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PMID:[Clinical estimation of 1-alpha-hydroxycholecalciferol in treatment of patients with chronic renal failure]. 130 33

One of the most endearing characters in English literature is Tiny Tim, the crippled son of Ebenezer Scrooge's clerk, Bob Cratchit. Yet the nature of Tiny Tim's multifaceted and implicitly reversible illness is a mystery and open to debate and speculation. From details of the original manuscript and the eight film versions, it is possible to construct a differential diagnosis for Tim's short stature, asymmetric crippling disorder, and curious intermittent weakness that would lead to his death, if untreated, within a period of 1 year. Following the ghostly visitations, Scrooge vows to assist the struggling Cratchit family financially, thereby making available the best medical care money could buy. From review of pediatrics texts from 1830 to 1850, a recommended treatment plan would have included (1) general measures such as country air and exercise, and fish oils such as cod and halibut (vitamin D), and (2) specific treatments of tonics (containing combinations of belladonna, opium, sodium bicarbonate, sodium citrate, and potassium chloride) emphasizing alkalis, and splinting and bracing the limbs. Such treatments with vitamin D and alkalinization with sodium bicarbonate and sodium citrate suggest the plausible speculation that Tiny Tim had renal tubular acidosis (type I), a disorder that is characterized by growth failure and, if left untreated, complicated by osteomalacia with pathologic fractures, hypokalemic muscle weakness and periodic paralysis, nephrocalcinosis leading to renal failure, and death. I propose that Tiny Tim had distal renal tubular acidosis (type I).
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PMID:What was wrong with Tiny Tim? 835 13

Acute encephalopathy following treatment with ifosfamide and mesna was observed in 5 (4 women and 1 men) of 28 patients (17.8%), with advanced sarcoma, lymphoma or ovarian carcinoma. This appeared within 2 to 7 days following the first dose of ifosfamide treatment, and included mental status changes, urinary incontinence, weakness, seizure activity, altered consciousness and psychiatric manifestations. Three cases were fatal, while two patients recovered completely. Brain CT and morphometric studies were normal in all the patients. Associated findings were myelosuppression, renal failure and electrolyte alterations.
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PMID:Encephalopathy in ifosfamide-treated patients. 148 35

Two patients sustained a severe compartment syndrome of the lower limb after surgery under bloodless field for 1 h 25 min and 43 min and with a tourniquet pressure of 350 and 450 mm Hg, respectively. In both cases fasciotomies were performed as an emergency procedure shortly after the initial operation. Renal failure was avoided but functional deficiencies, peroneal weakness, and restricted movements of the ankle resulted in both cases. We conclude that when using a tourniquet, any pre- and postoperative swelling or stiffness of the muscles in the operation area should be noted, even if the recommended time or pressure limits are not exceeded. Immediate fasciotomies of the affected compartments should be considered if the diagnosis is suspected.
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PMID:Compartment syndrome of the lower limb caused by a tourniquet: a report of two cases. 149 3


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