Renal disease and acid-suppressing drugs

No comparative epidemiological data can be found in the literature on the renal safety of acid-suppressing drugs. We followed-up a cohort of close to 180,000 persons during periods of treatment and non-treatment with five anti-ulcer drugs to evaluate the risk of idiopathic acute renal failure and/or nephrotic syndrome. After reviewing medical records, five patients were found to be cases. Two presented with acute renal failure and three had nephrotic syndrome. Three cases occurred during periods of non-exposure to anti-ulcer drugs. Two cases occurred during current use of ranitidine: one of acute renal failure and one of nephrotic syndrome. No case was encountered during treatment with cimetidine, famotidine, nizatidine or omeprazole. The incidence of idiopathic renal disease in the general population was 1 per 100,000 person-years. The relative risk associated with use of acid-suppressing drugs was 1.8 (95% CI, 0.3-10.7) compared to non-use. These results do not suggest a major increased risk for acute renal injury and/or nephrotic syndrome associated with use of anti-ulcer drugs.     

序贯透析治疗肾功能衰竭合并急性左心力衰竭的临床应用

目的观察序贯透析对肾功能衰竭合并心力衰竭、肺水肿患者的治疗效果。方法对13例肾功能衰竭合并急性心力衰竭、肺水肿的患者行序贯透析疗法,观察其临床症状、体征,分析其疗效。结果痊愈7例,显效5例,有效1例,总有效率为100.0%。结论序贯透析能迅速缓解肾功能衰竭合并急性左心力衰竭患者的临床症状,改善患者的心功能状况,是抢救肾功能衰竭合并急性左心力衰竭的有效方法 。     

60例慢性肾衰竭合并急性左心衰竭的治疗体会

目的对慢性肾衰竭合并急性左心衰竭患者的临床治疗进行深入的总结探析。方法对60例各种原因所导致的慢性肾衰竭合并急性左心衰竭患者应用药物控制血压,并且采取减轻心脏后负荷、降低外周血管阻力、采用血液透析、机械通气等多种治疗方法,控制患者心衰。结果经过治疗,96．7％（58／60）的慢性肾衰竭合并急性左心衰竭的患者抢救成功。结论针对慢性肾衰竭合并急性左心衰竭的不同发病机制,给予患者相应的处理措施,对慢性肾衰竭合并急性左心衰竭患者生命质量的提高有着尤为重要的意义。     

Hypothyroidism is a predisposing factor for fenofibrate-induced rhabdomyolysis--patient report and literature review

A literature survey reveals that both lipid lowering drugs - statins and fibrates--and hypothyroidism are documented causes of muscle disorders including rhabdomyolysis leading to acute renal failure. We describe a case of fenofibrate monotherapy (Lipicard) induced dialysis dependent acute renal failure in an undiagnosed hypothyroid patient which is the first case to be reported from Sri Lanka. We strongly recommend that all patients who are receiving statins and/or fibrates should be screened for occult hypothyroidism which seems to aggravate the muscle damage due to the above drugs, with or without other risk factors.     

Reversible renal failure associated with ibuprofen: case report and review of the literature

A report of a probable case of acute, reversible renal failure and hyperkalemia, after an increase in dose of ibuprofen, is presented. Other cases of renal dysfunction associated with various nonsteroidal antiinflammatory drugs (NSAIDs) are reviewed. The ability of NSAIDs to inhibit prostaglandin synthesis may explain the various renal consequences. Possible predisposing factors to renal deterioration include the amount of drug consumed, presence of compromised renal blood flow, underlying renal insufficiency, nephrotoxic drug combinations, and high urinary prostaglandin excretion. Generally, the renal failure with NSAIDs is acute and reversible, though analgesic nephropathy with papillary necrosis and chronic renal failure are reported. Electrolytes, blood urea nitrogen, and serum creatinine levels need to be monitored in high-risk patients with predisposing factors and for chronic, long-term use of drugs that inhibit prostaglandin synthesis.     

Chronic renal failure as a complication of hemorrhagic fever with renal syndrome in 17 years’ old boy

Hemorrhagic fever with renal syndrome (HFRS) is an acute infective multisystemic disease that commonly presents with fever, hemorrhage and acute renal failure. A 17-year-old boy presented with thrombocytopenia, profuse subconjunctival hemorrhage and anuric renal failure with fluid overload. The patient required continuous ambulatory peritoneal dialysis. He developed diuresis but did not recover renal function during reconvalescent period. Hantaan, Puumala, Seoul, Belgrade virus infection with haemorrhagic fever with renal syndrome was confirmed by serologic test.     

Mibefradil is more effective than verapamil for restoring post-ischemic function of isolated hearts of guinea pigs with acute renal failure

The deleterious intracellular Ca(2+) overload in the ischemic-reperfusion injury of the heart can be even more expressed in subjects with acute renal failure in whom maintenance of intracellular Ca(2+) has already been disturbed in normoxia. To study the influence of acute renal failure in ischemic-reperfusion injury on the heart, we used isolated Langendorff's hearts of guinea pigs with gentamicin-induced acute renal failure. We examined arrhythmias, heart contractility and myocardial cell damage during reperfusion. Two specific Ca(2+) channel antagonists, mibefradil (0.1 and 1 microM) and verapamil (0.1 microM), were used to test the possible involvement of T-type and L-type Ca(2+) channels in these processes. We exposed hearts to 50 min of zero-flow global ischemia and 60 min of reperfusion. During reperfusion, unrecoverable ventricular fibrillation appeared more often in hearts of animals with acute renal failure than in control hearts (80% vs. 0%, respectively). Mibefradil, but not verapamil, applied either pre- or post-ischemically, terminated ventricular fibrillation in all hearts of animals with acute renal failure. Mibefradil (0.1 microM only) improved contractility in hearts of animals with acute renal failure during reperfusion by 30%. During reperfusion, lactate dehydrogenase (LDH) release rate increased less in hearts of guinea pigs with acute renal failure than in control hearts and only verapamil decreased it additionally. Thus, our results suggest a more important role of T- than of L-type Ca(2+) channels in ischemic-reperfusion injury in isolated guinea pig hearts with acute renal failure.     

Acute Renal Failure After Administration of Intravenous Immunoglobulin: Review of the Literature and Case Report

Within in last 7 years the literature has published several reports of acute renal failure after the administration of intravenous immunoglobulin. Review of these cases finds that all occurrences in the United States except one involved a sucrose-containing immunoglobulin preparation, leading to the suspicion that sucrose may be the cause of the renal failure. Further investigation found that approximately 50 years ago, when sucrose was used as an osmotic diuretic, investigators reported acute renal failure in humans after intravenous infusions of 50 g or more. A patient at our institution developed acute renal failure similar to that described in published case reports after being administered a sucrose-containing immunoglobulin.     

Drug-induced renal disease.

The clinical manifestations of drug-induced renal disease may include all the manifestations attributed to natural or spontaneous renal diseases such as acute renal failure, chronic renal failure, acute nephritic syndrome, renal colic, haematuria, selective tubular defects, obstructive nephropathy, etc. It is therefore vital in any patient with renal disease whatever the clinical manifestations might be, to obtain a meticulous drug and toxin inventory. Withdrawal of the offending drug may result in amelioration or cure of the renal disorder although in the case of severe renal failure it may be necessary to utilise haemodialysis or peritoneal dialysis to tide the patient over the period of acute renal failure. Analgesic nephropathy is an important cause of terminal chronic renal failure and it is therefore vital to make the diagnosis as early as possible. The pathogenesis of some drug-induced renal disorders appears to be immunologically mediated. There are many other pathogenetic mechanisms involved in drug-induced renal disorders and some drugs may under appropriate circumstances be responsible for a variety of different nephrotoxic effects. For example, the sulphonamides have been incriminated in examples of crystalluria, acute interstitial nephritis, acute tubular necrosis, generalised hypersensitivity reactions, polyarteritis nodosa and drug-induced lupus erythematosus.     

Acute renal failure during lisinopril and losartan therapy for proteinuria

The use of combined therapy with an angiotensin-converting enzyme (ACE) inhibitor and an angiotensin II receptor blocker (ARB) for treatment of proteinuria has been gaining support. Limited data are available regarding this treatment in the pediatric population. This report describes a case of acute compromise of renal function associated with hypotension in a 7-year-old boy treated with the ACE inhibitor lisinopril and the ARB losartan. It emphasizes the need for close surveillance of renal function and blood pressure during such therapy even in patients with relative preservation of renal function. Further investigation into the utility and safety of dual therapy with an ACE inhibitor plus an ARB in pediatric patients is warranted. Key Words: renal failure, proteinuria, angiotensin-converting enzyme inhibitor, ACEI, angiotensin II receptor blocker, ARB.     

Involvement of nitric oxide in the suppressive effect of 17beta-estradiol on endothelin-1 overproduction in ischemic acute renal failure

It is known that 17beta-estradiol (E2-beta) increases the production of nitric oxide. We have demonstrated that E2-beta prevents renal injury and suppresses renal endothelin-1 overproduction in ischemic acute renal failure in rats. In the present study, we investigated whether N(G)-nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor, can reverse the effect of E2-beta in ischemic acute renal failure. Ischemic acute renal failure was induced by clamping the left renal artery and vein for 45 minutes followed by reperfusion, 2 weeks after contralateral nephrectomy. Pre-ischemic treatment with E2-beta (100 microg/kg, intravenously) attenuated the ischemia/ reperfusion-induced renal dysfunction and suppressed the increment of renal endothelin-1 content 24 hours after reperfusion. The effects of E2-beta on renal dysfunction and increased endothelin-1 content in acute renal failure rats were reversed by pretreatment with N(G)-nitro-L-arginine methyl ester (0.3 mg/kg, intravenously). An in vivo microdialysis study revealed that the concentration of nitric oxide metabolites in the kidney was reduced during ischemia, and quickly recovered after reperfusion in E2-beta-treated acute renal failure rats, compared with cases in untreated acute renal failure rats. This recovery of renal nitric oxide metabolite concentration with E2-beta was abolished by the pretreatment with N(G)-nitro-Larginine methyl ester. These findings suggest that nitric oxide is closely related to suppressive effect of E2-beta on renal endothelin-1 overproduction in acute renal failure rats and this suppression is probably involved in the beneficial effect of E2-beta on ischemia/reperfusion-induced renal injury.     

Diuretics induced uremia and nonrecovery of renal function in a patient with acute renal failure caused by sepsis

Sepsis is a clinical syndrome related to severe infection and is characterized by systemic inflammation and injury to multiple organs and functional systems. Sepsis is one of the main causes of acute renal failure (ARF). Diuretics are frequently administered during ARF. However, there is scant evidence that diuretics provide any benefit to the patients with ARF. This case report highlights the occurrence of uremia and nonrecovery of renal function after administration of diuretics in a patient with ARF caused by sepsis. It is suggested that physicians should be cautious in prescribing diuretics to patients with ARF due to septicemia. Diuretics cause uremia and may lead to false diagnosis of chronic renal failure and nonrecovery of renal function. The patient may unnecessarily require prolonged dialysis.     

Scrotal ulceration as a consequence of all-trans-retinoic acid (ATRA) for the treatment of acute promyelocytic leukemia

Induction therapy with all-trans-retinoic acid (ATRA), an oral vitamin A derivative, has been shown to improve the short and long-term outcome of patients with acute promyelocytic leukemia (APML). Common side effects include headache, fever, dry skin, and bone pain, and approximately 25% of treated patients experience ATRA syndrome, which includes fever, dyspnea, weight gain, pulmonary infiltrates, and pleural or pericardial effusions. Scrotal ulcerations due to ATRA are rare with 16 previously documented cases, most of whom were Asian. We report a Caucasian male with APML who developed scrotal ulceration during ATRA induction therapy and review the previously reported cases. Physicians and patients should be aware of this disturbing, but self-limited, dermatologic complication of ATRA.     

连续性静脉-静脉血液滤过治疗小儿急性肾功能衰竭

目的观察连续性静脉-静脉血液滤过(CVVEF)在小儿急性肾功能衰竭中的疗效,寻找安全有效的小儿急性肾功能衰竭的治疗方法。方法对2002-06～2008-03行该种连续性血液滤过治疗的16例小儿急性肾功能衰竭患者进行回顾性分析,对比观察治疗前后血肌酐、尿素氮、电解质、二氧化碳结合率、心率、血压的变化及不良反应的发生。结果16例患者中,12例完全治愈;3例达到临床治愈(尿蛋白持续1+～2+,肾功能完全恢复正常);1例病死,死亡原因与就诊过晚,延误治疗有关。结论连续性血液滤过可明显降低小儿急性肾功能衰竭病死率,是安全可行的治疗方法之一。     

Postpartum acute renal failure in a drug addict

Renal diseases occur in intravenous drug abusers, especially heroin addicts, in the form of interstitial nephritis, nephrotic syndrome or acute renal failure due to rhabdomyolysis. We report a case of acute renal failure not ascribable to rhabdomyolysis nor to the main pathogenetic mechanisms of pregnancy-related acute renal failure in a pregnant heroin addict woman after vaginal delivery following uncomplicated pregnancy. Drug-related immunological abnormalities and microcirculatory distress may be involved.     

连续性肾脏替代治疗在心脏术后急性肾衰中的应用

目的研究连续性静脉－静脉血液透析滤过（ＣＶＶＨＤＦ）治疗以及术后并发急性肾功能衰竭（ＡＲＦ）的疗效。方法对４例心脏术后并发ＡＲＦ的患，采用ＰＲＩＳＭＡ（Ｈｏｓｐａｌ）床旁血透机行连续静脉静脉血液透析滤过。结果对４例患，死亡３例，存活１例。用ＣＶＶＨＤＦ治疗３０ ｍｉｎ后，平均动脉压显上升，心率则显减慢。治疗８ｈ后，血清Ｎａ＾＋、ＣＬ＾－、Ｃａ＾２＋和动脉血气中ｐＨ值均无显变化，但血清ＢＵ     

Acute pancreatitis and acute renal failure complicating doxylamine succinate intoxication

Doxylamine succinate is an antihistaminic drugwith additional hypnotic, anticholinergic and local anesthetic effects first described in 1948. In Korea and many other countries, it is a common-over-the counter medication frequently involved in overdoses. Clinical symtomatology of doxylamine succinate overdose includes somnolence, coma, seizures, mydriasis, tachycardia, psychosis, and rhabdomyolysis. A serious complication may be rhabdomyolysis with subsequent impairment of renal function and acute renal failure. We report a case of acute renal failure and acute pancreatitis complicating a doxylamine succinate intoxication.     

URODILATIN (INN: ULARITIDE) AS A NEW DRUG FOR THE THERAPY OF ACUTE RENAL FAILURE FOLLOWING CARDIAC SURGERY

1. Acute renal failure is a severe complication following major cardiac surgery. 2. The effects of urodilatin were evaluated in a randomized, double-blind trial in patients suffering from incipient acute renal failure following cardiac surgery. 3. In the urodilatin group (n= 7) acute renal failure was reverted, whereas in the placebo group (n= 7) six patients had to be haemofiltered or haemodialysed (P < 0.005). 4. Urodilatin induced a rapid onset of diuresis in contrast to placebo-treated patients, who remained oliguric. 5. In the placebo group four of seven patients died while still on haemodialysis (mortality rate 57.1 %) during a postoperative follow-up period of 60 days, while all patients treated with urodilatin survived. 6. On the basis of these results it would appear that urodilatin is an effective drug for the treatment of incipient oliguric acute renal failure following cardiac surgery and for avoiding haemodialysis/haemoflltration.     

The role of renal sympathetic nervous system in the pathogenesis of ischemic acute renal failure

We investigated the role of renal sympathetic nervous system in the progression of ischemia/reperfusion-induced acute renal failure in rats. Acute renal failure was induced by clamping the left renal artery and vein for 45 min followed by reperfusion, 2 weeks after the contralateral nephrectomy. Renal venous plasma norepinephrine concentrations markedly and significantly increased immediately after reperfusion, thereafter, the increased level declined but remained higher even at 24 h after reperfusion. Renal sympathetic nerve activity was significantly augmented during the renal ischemia. Renal denervation or the administration of pentolinium, a ganglion blocking agent, (5 mg/kg i.v.) at 5 min before ischemia attenuated the ischemia/reperfusion-induced renal dysfunction and histological damage, such as proteinaceous casts in tubuli and tubular necrosis. The elevation of renal venous norepinephrine levels after reperfusion was suppressed by renal denervation or pentolinium treatment. Thus, a surgical or pharmacological blockade of renal sympathetic nerve prevents the progression of ischemia/reperfusion-induced acute renal failure, thereby suggesting that renal sympathetic nervous system plays an important role in the development of the ischemic acute renal failure.     

Pharmacological studies on diuretic action of azosemide [5-(4'-chloro-5'-sulfamoyl-2'-thenylamino)-phenyltetrazole], a new diuretic (2). Diuretic action of azosemide in HgCl2-induced acute renal failure in rats

The diuretic effect of azosemide in HgCl2-induced acute renal failure of rats was investigated in comparison with that of furosemide. Acute renal failure was induced by the single s.c. injection of 1, 2, or 4 mg/kg HgCl2; and the test drug was administered 48 hr after treatment with HgCl2. Treatment with HgCl2 resulted in a dose related elevation of plasma urea nitrogen and creatinine levels (mg/dl). In rats with 1 mg/kg HgCl2-induced acute renal failure, azosemide at doses ranging from 10 to 40 mg/kg p.o. dose-dependently increased urinary volume (ml/5 hr) and urinary Na+, K+, and Cl- excretions (mEq/5 hr). In this case, azosemide at 40 mg/kg caused a 3.5-fold increase in urinary volume and 4.5-, 2.1, and 4.1-fold increases in urinary Na+, K+, and Cl- excretions, respectively. Although plasma electrolyte levels were little affected by azosemide, plasma urea nitrogen and creatinine levels were significantly elevated by doses of more than 20 mg/kg of this drug. The diuretic effect of azosemide was more markedly reduced in rats with 2 mg/kg HgCl2-induced acute renal failure than in rats with 1 mg/kg HgCl2-induced acute renal failure. In the case of treatment with HgCl2 of 2 mg/kg, the diuretic effect of azosemide at doses ranging from 40-320 mg/kg p.o. was dose-dependent. However, azosemide had no effect on plasma electrolyte, urea nitrogen, and creatinine levels. The diuretic effect of azosemide in rats given 4 mg/kg HgCl2 was more pronouncedly reduced as compared with that in the case of 2 mg/kg HgCl2. In this case, azosemide at 320 mg/kg brought about a 2.6-fold increase in urinary volume and 4.8-, 4.6-, and 3.9-fold increases in urinary Na+, K+, and Cl- excretions, respectively. This drug had no effect on any plasma parameters. The diuretic effect of azosemide was slightly more potent than those of furosemide in the case of acute renal failure induced by 2 and 4 mg/kg HgCl2.