No abstract available.
Antineoplastic Agents/*adverse effects ; Female ; Humans ; Indoles/*adverse effects ; Male ; Proteinuria/*chemically induced ; Pyrroles/*adverse effects ; Renal Insufficiency/*chemically induced

Chronic Disease ; Female ; Humans ; Lead Poisoning ; complications ; Middle Aged ; Occupational Diseases ; Renal Insufficiency ; chemically induced

Amoxicillin ; adverse effects ; Anti-Bacterial Agents ; adverse effects ; Child ; Humans ; Male ; Renal Insufficiency ; chemically induced

Colchicine plays an important role in the treatment of gout and some other diseases. Besides gastrointestinal symptoms, myopathy has been reported as a rare side effect of colchicine in some patients. We report a case of myopathy in a patient with chronic kidney disease caused by high-dose colchicine, and then review literature on colchicine-induced myopathy, so as to provide some experience for the clinical diagnosis, treatment and medication safety. A 51-year-old male patient with 10 years of gout and 5 years of chronic kidney disease history and irregular treatment was admitted to the hospital with complaint of recurrent left wrist arthralgia and emerging lower extremities myalgia after intake of 40-50 mg colchicine in total within 20 days. Laboratory examinations showed significantly increased creatine kinase (CK) and then colchicine-induced myopathy was diagnosed preliminarily. After withdrawl of colchicine and implementation of hydration, alkalization and intramuscular injection of compound betamethasone, the symptoms of arthralgia and myalgia were relieved within 3 days and CK decreased to normal range gradually. According to literature reports, colchicine related myopathy was mostly characterized by proximal myasthenia and myalgia, accompanied by elevated CK level, which usually occurred days to weeks after initial administration of colchicine at the usual dosage in patients with renal impairment or a change in the underlying disease state in those receiving long-term therapy, and the features might remit within three to four weeks after the drug was discontinued. Electromyography of proximal muscles showed myopathy marked by abnormal spontaneous activity and muscle pathology waa marked by accumulation of lysosomes and autophagic vacuoles. Chronic kidney disease, liver cirrhosis, higher colchicine dose and concomitant cytochrome P450 3A4 (CYP3A4) inhibitors were associated with increased risk of myo-pathy. Based on the similar efficacy and lower adverse reaction rate compared with larger dosage, small dose of colchicine was recommended by many important current guidelines and recommendations in the treatment of gout. In consideration of potential risks, colchicine should be used with caution in patients with kidney or liver impairment, and in those taking CYP3A4 or P-glycoprotein inhibitors. For those patients, the drug dose should be adjusted and the latent adverse reactions should be monitored carefully.
Colchicine/adverse effects* ; Gout/drug therapy* ; Humans ; Kidney ; Male ; Middle Aged ; Muscular Diseases/chemically induced* ; Renal Insufficiency, Chronic/complications*

Drug-induced nephrotoxicity is very common in both new drug development and clinic practice. Various drugs can induce kidney injuries, including tubulointerstitial, glomerular and renal vascular disease. To investigate the mechanism of drug induced nephrotoxicity is important for risk reduction of new drug development, reasonable drug usage, early discovery and effective prevention/treatment of adverse effects in clinics.
Acute Kidney Injury ; chemically induced ; Animals ; Anti-Infective Agents ; adverse effects ; Anti-Inflammatory Agents, Non-Steroidal ; adverse effects ; Antineoplastic Agents ; adverse effects ; Humans ; Immunosuppressive Agents ; adverse effects ; Kidney Diseases ; chemically induced ; Kidney Tubular Necrosis, Acute ; chemically induced ; Nephritis, Interstitial ; chemically induced ; Renal Insufficiency ; chemically induced

The article summarized the general situation of the study on the renal toxicity caused by aristolochic acids (AAs) and Chinese herbs containing AAs. The renal lesion induced by AAs and Chinese herbs containing AAs locates mainly in renal tubules, and glomeruluses have no obvious histological change. The short term administration of large doses causes acute renal epithelia denaturalization and tubular necrosis, but the long-term administration may result in chronically progressive interstitial fibrosis of the kidney. Renal failure may occur following both acute and chronic renal lesion. The renal function should be strictly monitored while one is using the Chinese herbs containing AAs, and the dosage and duration for the treatment must be limited to prevent renal toxicity.
Animals ; Aristolochiaceae ; chemistry ; Aristolochic Acids ; adverse effects ; isolation & purification ; toxicity ; Drugs, Chinese Herbal ; adverse effects ; isolation & purification ; toxicity ; Fibrosis ; Humans ; Kidney ; pathology ; Kidney Tubules ; pathology ; Nephritis, Interstitial ; chemically induced ; pathology ; Plants, Medicinal ; chemistry ; Renal Insufficiency ; chemically induced

OBJECTIVETo investigate the clinical and pathological characteristics of bevacizumab-induced renal impairment.

METHODThe clinical and pathological data of 4 patients with bevacizumab-induced renal impairment in Peking Union Medical College Hospital was retrospectively analyzed.

RESULTSThere were 2 men and 2 women aged (56.5±11.5) years. Before bevacizumab treatment, three non-small cell lung cancer patients (75%) had normal renal function and only one pancreatic cancer patient (25%) had mild renal impairment. After 2-14 cycles of bevacizumab treatment, the most common clinical manifestation of bevacizumab-induced renal injury was proteinuria (>3.5 g/d) (n=4, 100%). Other clinical symptoms included microscopic hematuria (n=2, 50%), malignant hypertension (n=1, 25%), elevated serum creatinine level as accompanied with acute renal failure (n=1, 25%), and anuria (n=1, 25%). Thrombotic microangiopathy was the main pathological type (n=2, 50%), whereas other pathological types included membranoproliferative glomerulonephritis (n=1, 25%) and benign arteriolar nephrosclerosis (n=1, 25%). After the detection of renal impairment, bevacizumab therapy was stopped in all 4 cases (100%). Hemodialysis was performed in the patient with acute renal failure. The prognosis was relatively good. The renal function and proteinuria was completely recovered in one patient (25%), whereas the other three patients (75%) presented with persistent alleviated proteinuria but normal renal function.

CONCLUSIONSBevacizumab may cause renal injury via complex mechanisms. Therefore, urine protein excretion and renal function should be closely monitored during bevacizumab treatment to identify any renal injury. The prognosis is relatively good after discontinuation of bevacizumab.

Adult ; Aged ; Antibodies, Monoclonal, Humanized ; adverse effects ; Bevacizumab ; Female ; Humans ; Kidney ; drug effects ; pathology ; Male ; Middle Aged ; Renal Insufficiency ; chemically induced ; pathology ; Retrospective Studies

Cerebellitis is a rarely encountered complication of isoniazid therapy. Its occurrence is usually associated with concomitant renal disease and haemodialysis. Herein, we report the case of a patient with this complication who presented with isolated bilateral symmetrical dentate nucleus T2 hyperintensities on magnetic resonance imaging. Isoniazid neurotoxicity has never been reported to cause bilateral dentate hyperintensities, for which the differentials are few and include metronidazole toxicity.
Adult ; Antitubercular Agents ; adverse effects ; Cerebellar Diseases ; chemically induced ; Cerebellar Nuclei ; pathology ; Diagnosis, Differential ; Female ; Humans ; Isoniazid ; adverse effects ; Magnetic Resonance Imaging ; Renal Dialysis ; Renal Insufficiency ; therapy ; Tuberculosis ; drug therapy

BACKGROUND/AIMS: Sunitinib is an oral multitargeted tyrosine kinase inhibitor used mainly for the treatment of metastatic renal cell carcinoma. The renal adverse effects (RAEs) of sunitinib have not been investigated. The aim of this study was to determine the incidence and risk factors of RAEs (proteinuria [PU] and renal insufficiency [RI]) and to investigate the relationship between PU and antitumor efficacy. METHODS: We performed a retrospective review of medical records of patients who had received sunitinib for more than 3 months. RESULTS: One hundred and fifty-five patients (mean age, 58.7 +/- 12.6 years) were enrolled, and the mean baseline creatinine level was 1.24 mg/dL. PU developed in 15 of 111 patients, and preexisting PU was aggravated in six of 111 patients. Only one patient developed typical nephrotic syndrome. Following discontinuation of sunitinib, PU was improved in 12 of 17 patients but persisted in five of 17 patients. RI occurred in 12 of 155 patients, and the maximum creatinine level was 3.31 mg/dL. RI improved in two of 12 patients but persisted in 10 of 12 patients. Risk factors for PU were hypertension, dyslipidemia, and chronic kidney disease. Older age was a risk factor for RI. The median progression-free survival was significantly better for patients who showed PU. CONCLUSIONS: The incidence of RAEs associated with sunitinib was lower than those of previous reports. The severity of RAEs was mild to moderate, and partially reversible after cessation of sunitinib. We suggest that blood pressure, urinalysis, and renal function in patients receiving sunitinib should be monitored closely.
Aged ; Antineoplastic Agents/*adverse effects ; Carcinoma, Renal Cell/complications/drug therapy/mortality ; Female ; Humans ; Incidence ; Indoles/*adverse effects ; Kidney Neoplasms/complications/drug therapy/mortality ; Male ; Middle Aged ; Proteinuria/*chemically induced/epidemiology ; Pyrroles/*adverse effects ; Renal Insufficiency/*chemically induced/epidemiology ; Republic of Korea/epidemiology ; Retrospective Studies ; Risk Factors ; Treatment Outcome

OBJECTIVETo investigate the effects of marine collagen peptide on adenine-induced chronic renal function impairment in rats.

METHODSAdenine suspension (100 mg/kg ) was given to Sprague-Dawley rats to made the model of renal function impairment. Marine collagen peptide 1.125 g x kg(-1) x d(-1) and 2.25 g x kg(-1) x d(-1) were administered intragastricly in two intervention groups. In addition, adenine suspension (100 mg/kg ) was given. Experiment was kept 12 weeks. Time-dependent levels of serum creatinine (Cr), urea nitrogen (BUN) and creatinine clearance rate were monitored. Kidney ultramicrostructure was checked through transmission electron microscope.

RESULTSIn model group, level of serum Cr, BUN and Ccr of 5, 8, 12th week respectively were: (182.2 +/- 119.52, 308.17 +/- 88.37, 347.57 +/- 68.24; 29.20 +/- 16.48, 63.03 +/- 18.68, 95.53 +/- 24.88; 0.53 +/- 0.23, 0.17 +/- 0.13, 0.14 +/- 0.08). Serum Cr, BUN levels in marine collagen peptide 2.25 g x kg(-1) x d(-1) treated rats were lower and Ccr was higher significantly than that of model group. Level of serum Cr, BUN and Ccr of 5, 8, 12th week in marine collagen peptide treatment group respectively were: (105.60 +/- 11.84, 175.40 +/- 73.93, 240.14 +/- 71.53; 23.62 +/- 3.89, 41.90 +/- 23.78, 72.93 +/- 26.12; 0.99 +/- 0.35, 0.45 +/- 0.28, 0.26 +/- 0.06). Besides, kidney ultramicrostructure damage was ameliorated. Favorable effect of marine collagen peptide 1.125 g x kg(-1) x d(-1) was also observed on renal function impairment, but the difference compared to model group was not significant.

CONCLUSIONMarine collagen peptide at a dose of 2.25 g x kg(-1) x d(-1) might slow down the progression of chronic renal function impairment induced by adenine in rats.

Adenine ; adverse effects ; Animals ; Collagen ; administration & dosage ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Male ; Marine Biology ; Peptides ; administration & dosage ; Rats ; Rats, Sprague-Dawley ; Renal Insufficiency, Chronic ; chemically induced ; prevention & control