The peroxisome proliferator-activated receptors (PPARs) are nuclear fatty acid receptors, which contain a type II zinc finger DNA binding motif and a hydrophobic ligand binding pocket. These receptors are thought to play an important role in metabolic diseases such as obesity, insulin resistance, and coronary artery disease. Three subtypes of PPAR receptors have been described: PPARα, PPARδ/β, and PPARγ. PPARα is found in the liver, muscle, kidney, and heart. In the liver, its role is to up-regulate genes involved in fatty acid uptake, binding, β-oxidation and electron transport, and oxidative phosphorylation in subcutaneous fat but not in skeletal muscle. PPARδ/β is expressed in many tissues but markedly in brain, adipose tissue, and skin. PPARγ has high expression in fat, low expression in the liver, and very low expression in the muscle. The thiazolidinediones (TZD) are synthetic ligands of PPARγ. By activating a number of genes in tissues, PPARγ increases glucose and lipid uptake, increases glucose oxidation, decreases free fatty acid concentration, and decreases insulin resistance. Although, there is a rationale for the use of TZDs in patients with type 2 diabetes mellitus, clinical studies have produced conflicting data. While currently used TZDs are clearly associated with heart failure (HF) worsening; with regards to cardiovascular outcomes, pioglitazone seems to be related to a trend toward reduction in cardiovascular morbidity and mortality, whereas rosiglitazone may actually increase risk of cardiovascular events. We review the existing literature on TZDs and discuss role and cardiovascular safety of these agents for the contemporary treatment of diabetes. Other side effects of these agents i.e. increase in osteoporosis and possible risk of bladder cancer is also discussed.
Background: Ethylene glycol ingestion can lead to acute kidney injury from tubular deposition of oxalate crystals. The diagnosis of ethylene glycol intoxication is based on a history of ingestion, clinical examination, high anion gap metabolic acidosis, high osmolal gap, and a measured serum level of ethylene glycol. However, depending on the delay in time from ingestion to arrival to a hospital, the osmolal gap may become normal, thereby creating a confusing clinic picture for the treating clinician. Case: A 71 year-old man with a history of alcohol abuse had been unconscious for an unknown period of time. Upon hospitalization, he was found to have a high anion gap metabolic acidosis but a normal serum osmolal gap and subsequently developed acute kidney injury. The serum lactic acid and glucose levels were unremarkable, and there were no ketones in the serum. Urine analysis showed numerous red blood cells and calcium oxalate crystals. The renal biopsy showed multiple oxalate crystals in the renal tubules demonstrating birefringence under polarized light. Given the history of alcohol abuse, the clinical presentation, the unexplained high anion gap metabolic acidosis, and the biopsy findings, ethylene glycol intoxication was deemed the most likely diagnosis. Conclusions: In cases of ethylene glycol intoxication, a high serum osmolal gap is supportive of ethylene glycol intoxication, but a normal serum osmolal gap does not exclude the diagnosis, especially when the time of ingestion is unknown. Physicians should be aware of potentially normal serum osmolal gap values in cases of ethylene glycol intoxication. Implication for health policy/practice/research/medical education:Physicians should be aware of potentially normal serum osmolal gap values in cases of ethylene glycol intoxication. In the appropriate clinical setting consistent with ethylene glycol intoxication, a normal serum osmolal gap should not be relied upon to exclude the diagnosis and withhold checking the ethylene glycol serum level and treatment.Please cite this paper as: Alhamad T, Blandon J, Meza AT, Bilbao JE, Hernandez GT. Acute kidney injury with oxalate deposition in a patient with a high anion gap metabolic acidosis and a normal osmolal gap.
Contrast-induced acute kidney injury is one of the leading causes of hospital-acquired acute kidney injury. Thus far, no strategies have been clearly shown to be effective in preventing contrast-induced acute kidney injury beyond thorough patient selection, meticulous hydration of the patient, and minimizing the amount of contrast used. Additional studies are needed to define the optimal means of hydration, role of commonly advocated prophylaxis strategies such as N-acetylcysteine and develop newer more novel effective therapies to prevent or minimize the risk of kidney injury.
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