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Perioperative acute kidney injury (AKI) is associated with increased morbidity and mortality. Patient comorbidities, the type of surgery, timing of surgery, and exposure to nephrotoxins are important contributors for developing acute kidney injury. Urgent or emergent surgery, cardiac, and organ transplantation procedures are associated with a higher risk of acute kidney injury. Nephrotoxic drugs, contrast dye, and diuretics can worsen preexisting kidney dysfunction or act as an additive and/or synergistic insult to perioperative injury. A history of preoperative chronic kidney disease is the main risk factor for developing AKI, conferring as much as a 10-fold risk. However, beyond the preoperative renal function, the development of AKI is a complex phenomenon that involves a combination of patient-related and surgery-related factors., Competing Interests: Declaration of Competing Interest None., (Published by Elsevier Ltd.)

The milk-alkali syndrome became rare with the advent of modern ulcer therapy with nonabsorbable antacids, histamine2 blockers, and sucralfate. An increased frequency of this syndrome seems likely with the growing popularity of the use of calcium carbonate as an antacid or as calcium supplementation to prevent osteoporosis. We treated five patients who had six episodes of the milk-alkali syndrome; four of these cases were diagnosed between 1990 and 1992. All patients were ingesting massive quantities of calcium and absorbable alkali and were unaware of the toxic effects of these compounds. All patients presented with the triad of hypercalcemia, metabolic alkalosis, and renal failure. All metabolic abnormalities were corrected, and renal function improved with appropriate supportive measures and cessation of calcium and alkali ingestion. In two patients, the renal failure was so severe that dialysis was necessary. In four patients, either the serum amino-terminal parathyroid hormone or 1,25-dihydroxycholecalciferol levels were appropriately decreased in response to hypercalcemia. The serum carboxy-terminal parathyroid hormone levels were increased because of renal failure. Since both physicians and patients are often unaware of the calcium and alkali content of many nonprescription medicines, the diagnosis of the milk-alkali syndrome, a reversible cause of renal failure, can be missed if a detailed history of such intake is not elicited. Measurement of the serum amino-terminal parathyroid hormone and 1,25-dihydroxycholecalciferol levels may help differentiate milk-alkali syndrome from primary hyperparathyroidism.

To identify factors that may explain the persistently high mortality of acute renal failure (ARF), we compared the cause, clinical course, and outcome of 55 consecutive patients with ARF who underwent hemodialysis (HD) from 1962 to 1969 with 46 similar patients from 1979 to 1981 at the same medical center. We noted an overall increase in mortality from 54.5% to 71.7%. There was an increase in the number of elderly patients developing ARF, but age per se did not influence survival. There was a significant increase in mortality in younger patients resulting from the severity of their underlying illness. We saw an increase in the number of complicating factors occurring at the onset of ARF that correlated with the increase in mortality. In survivors ARF was more prolonged in our most recent experience. The development of prolonged, complicated ARF and the poor survival seen in younger patients led to the increase in mortality in our patients.