ABSTRACT
BACKGROUND/AIMS: Hypocalcemia is an important complication of rhabdomyolysis for which several pathogenic factors, including acute kidney injury (AKI), have been proposed. To gain insight regarding the hypocalcemic roles of AKI in rhabdomyolysis, we retrospectively examined patients with rhabdomyolysis. METHODS: Of 28,387 patients admitted to the Department of Internal Medicine, 51 patients met the inclusion criteria for the study. Serum calcium was analyzed based on laboratory data including indicators of AKI, serum creatine kinase (CK) and serum inorganic phosphate (iP). RESULTS: Twenty-two patients (43%) had hypocalcemia. Compared with patients without hypocalcemia, they had a higher prevalence of AKI (82 vs. 55%; p = 0.046), higher levels of peak CK (39,100 ± 50,600 vs. 9,800 ± 11,900 IU/l; p = 0.003) and higher levels of peak iP (1.77 ± 1.10 vs. 1.10 ± 0.35 mmol/l; p = 0.007). Indicators of AKI were correlated with peak CK and peak iP and were not significant variables in the regression analysis for hypocalcemia. Peak CK and peak iP were not correlated with each other. Impaired phosphate use by muscle contributed to the increased iP. CONCLUSION: These findings indicate that muscle damage is the primary hypocalcemic factor in rhabdomyolysis. AKI facilitated hypocalcemia by exacerbating the hyperphosphatemic effects of muscle damage. Aggressive hydration, which could increase oxygen supply and subsequently repair phosphate use in muscle, might reduce the incidence of hypocalcemia in rhabdomyolysis.
Subject(s)
Acute Kidney Injury/blood , Hyperphosphatemia/blood , Hypocalcemia/blood , Muscle, Skeletal/pathology , Rhabdomyolysis/pathology , Acute Kidney Injury/complications , Aged , Creatine Kinase/metabolism , Female , Humans , Hyperphosphatemia/etiology , Hypocalcemia/complications , Kidney Function Tests , Male , Middle Aged , Phosphates/blood , Prevalence , Retrospective Studies , Rhabdomyolysis/etiologyABSTRACT
Percutaneous endovascular angioplasty is a valuable tool to salvage dialysis vascular access failure, but is accident-prone if performed by unskilled operators. We report a case of vascular access failure caused by the plastic protective tube of a balloon catheter, which had been mistakenly left in the vasculature and was undetectable on radiography but was detected by ultrasonography.
Subject(s)
Catheters , Foreign Bodies/diagnostic imaging , Foreign Bodies/surgery , Kidney Failure, Chronic/therapy , Renal Dialysis/instrumentation , Aged , Equipment Failure , Humans , Male , UltrasonographyABSTRACT
An inhibition in the renin-angiotensin system (RAS) is one of the most widely used therapies to treat chronic kidney disease. However, its effect is occasionally not sufficient and additional treatments may be required. Recently, we reported that nicorandil exhibited renoprotective effects in a mouse model of diabetic nephropathy. Here we examined if nicorandil can provide an additive protection on enalapril in chronic kidney disease. Single treatment with either enalapril or nicorandil significantly ameliorated glomerular and tubulointerstitial injury in the rat remnant kidney while the combination of these two compounds provided additive effects. In addition, an increase in oxidative stress in remnant kidney was also blocked by either enalapril or nicorandil while the combination of the drugs was more potent. A mechanism was likely due for nicorandil to preventing manganase superoxide dismutase (MnSOD) and sirtuin (Sirt)3 from being reduced in injured kidneys. A study with cultured podocytes indicated that the antioxidative effect could be mediated through sulfonylurea receptor (SUR) in the mitochondrial KATP channel since blocking SUR with glibenclamide reduced MnSOD and Sirt3 expression in podocytes. In conclusion, nicorandil may synergize with enalapril to provide superior protection in chronic kidney disease.
Subject(s)
Angiotensin-Converting Enzyme Inhibitors/pharmacology , Antioxidants/pharmacology , Enalapril/pharmacology , Kidney/drug effects , Nicorandil/pharmacology , Renal Insufficiency, Chronic/drug therapy , Animals , Blood Pressure/drug effects , Cell Line , Disease Models, Animal , Drug Synergism , Drug Therapy, Combination , KATP Channels/drug effects , KATP Channels/metabolism , Kidney/metabolism , Kidney/pathology , Male , Mice , Nephrectomy , Oxidative Stress/drug effects , Podocytes/drug effects , Podocytes/metabolism , Podocytes/pathology , Potassium Channel Blockers/pharmacology , Rats, Sprague-Dawley , Renal Insufficiency, Chronic/etiology , Renal Insufficiency, Chronic/metabolism , Renal Insufficiency, Chronic/pathology , Sirtuin 3/metabolism , Sulfonylurea Receptors/drug effects , Sulfonylurea Receptors/metabolism , Superoxide Dismutase/metabolism , Time FactorsABSTRACT
Acetaminophen overdose can lead to severe liver and kidney failure; however, the risk of therapeutic doses in healthy individuals causing acute kidney injury (AKI) is less clear. We herein describe the cases of two young adults with renal biopsy-proven acute tubular necrosis under a therapeutic dose of acetaminophen. The first patient exhibited mild reversible renal insufficiency, whereas, in the second case, the patient demonstrated a slightly increased serum creatinine level and enlarged kidneys and the administration of contrast media and antibiotics may have worsened the renal dysfunction, leading to the need for temporal hemodialysis. Physicians should be aware of the risk of acetaminophen causing AKI and avoid administering other nephrotoxic agents in such cases.
