Effect of Transient and Sustained Acute Kidney Injury on Readmissions in Acute Decompensated Heart Failure.

Although acute kidney injury (AKI) is common in heart failure, yet the impact of the onset, timing, and duration of AKI on short-term outcomes is not well studied. AKI was defined as an increase in serum creatinine SCr of ≥0.3 mg/dl or 1.5 times relative to the admission and further categorized as transient AKI (T-AKI: SCr returning to within 10% of baseline); sustained AKI (S-AKI: those with at least 72 hours of hospital stay and did not meet T-AKI); and unknown duration AKI (U-AKI: those with less than 72 hours stay and did not meet T-AKI). Reference category was no AKI (stable or <0.3 mg/dl change in SCr). The main outcome was 30-day all-cause hospital readmission. Unadjusted and adjusted association between AKI category of interest and main outcome was represented as percent and relative risks with 95% CIs. Statistical significance was set at an alpha of 0.05. From the Cerner Health Facts sample, 14,017 of 22,059 available subjects met the eligibility criteria. Approximately, 19.2% of our sample met the primary outcome. Compared with no AKI (readmission rate of 17.7%; 95% CI 16.4% to 18.9%), the adjusted rate of readmission was highest in patients with S-AKI (22.8%, 95% CI 20.8% to 24.8%; p <0.001), followed by 20.2% (95% CI 17.5% to 22.8%; p = 0.05) in T-AKI patients. Compared with no AKI, the adjusted relative risk of 30-day readmission was 1.29 (95% CI 1.17 to 1.42), 1.14 (95% CI 1.00 to 1.31), and 1.12 (95% CI, 1.01 to 1.26) in S-AKI, T-AKI, and U-AKI, respectively. In conclusion, both sustained AKI and patients with transient elevation still remain at a higher risk of readmission within 30 days. Future studies should focus on examining process-of-care after discharge in patients with different patterns of AKI.

Renal sarcoidosis presenting as acute kidney injury with granulomatous interstitial nephritis and vasculitis.

Among the various renal manifestations of sarcoidosis, granulomatous inflammation confined to the tubulointerstitial compartment is the most commonly reported finding. We present the case of a 66-year-old man with acute kidney injury, hypercalcemia, mild restrictive pulmonary disease, and neurologic signs of parietal lobe dysfunction. Kidney biopsy showed diffuse interstitial inflammation with noncaseating granulomas that exhibited the unusual feature of infiltrating the walls of small arteries with destruction of the elastic lamina, consistent with granulomatous vasculitis. The findings of granulomatous interstitial nephritis on kidney biopsy, hypercalcemia, and possible cerebral and pulmonary involvement in the absence of other infectious, drug-induced, or autoimmune causes of granulomatous disease established the diagnosis of sarcoidosis. Pulse methylprednisolone followed by maintenance prednisone therapy led to improvement in kidney function, hypercalcemia, and neurologic symptoms. Vasculocentric granulomatous interstitial nephritis with granulomatous vasculitis is a rare and under-recognized manifestation of renal sarcoidosis.

Decongestive treatment of acute decompensated heart failure: cardiorenal implications of ultrafiltration and diuretics.

In patients with acute decompensated heart failure (ADHF), treatment aimed at adequate decongestion of the volume overloaded state is essential. Despite diuretic therapy, many patients remain volume overloaded and symptomatic. In addition, adverse effects related to diuretic treatment are common, including worsening kidney function and electrolyte disturbances. The development of decreased kidney function during treatment affects the response to diuretic therapy and is associated with important clinical outcomes, including mortality. The occurrence of diuretic resistance and the morbidity and mortality associated with diuretic therapy has stimulated interest to develop effective and safe treatment strategies that maximize decongestion and minimize decreased kidney function. During the last few decades, extracorporeal ultrafiltration has been used to remove fluid from diuretic-refractory hypervolemic patients. Recent clinical studies using user-friendly machines have suggested that ultrafiltration may be highly effective for decongesting patients with ADHF. Many questions remain regarding the comparative impact of diuretics and ultrafiltration on important clinical outcomes and adverse effects, including decreased kidney function. This article serves as a summary of key clinical studies addressing these points. The overall goal is to assist practicing clinicians who are contemplating the use of ultrafiltration for a patient with ADHF.

Management of hyponatremia: providing treatment and avoiding harm.

Hyponatremia, in its most severe form, requires urgent infusion of hypertonic saline to correct cerebral edema. However, overly rapid correction of chronic hyponatremia can cause osmotic demyelination syndrome. The authors review the treatment of hyponatremia in order to provide clinicians with a sound approach in a variety of settings in which severity, symptoms, and underlying disease states influence therapy. Also discussed is the current role of vasopressin antagonists in treatment.

Evaluation of hyponatremia: a little physiology goes a long way.

Hyponatremia is common in hospitalized patients. By taking a careful and logical approach, one can promptly recognize the causative factor or factors in nearly all cases. Most cases of hyponatremia are due to impaired renal water excretion, and recognizing the cause and pathophysiologic process makes it possible to provide focused individualized care and avoid mistreatment.

Cardiac troponins in renal insufficiency: review and clinical implications.

Patients with renal insufficiency may have increased serum troponins even in the absence of clinically suspected acute myocardial ischemia. While cardiovascular disease is the most common cause of death in patients with renal failure, we are just beginning to understand the clinical meaning of serum troponin elevations. Serum troponin T is increased more frequently than troponin I in patients with renal failure, leading clinicians to question its specificity for the diagnosis of myocardial infarction. Many large-scale trials demonstrating the utility of serum troponins in predicting adverse events and in guiding therapy and intervention in acute coronary syndromes have excluded patients with renal failure. Despite persistent uncertainty about the mechanism of elevated serum troponins in patients with reduced renal function, data from smaller groups of renal failure patients have suggested that troponin elevations are associated with added risk, including an increase in mortality. It is possible that increases in serum troponin from baseline in patients with renal insufficiency admitted to hospital with acute coronary syndrome may signify myocardial necrosis. Further studies are needed to clarify this hypothesis.

Distribution of Peyer's patches in the distal ileum.

BACKGROUND AND AIMS: Peyer's patches play a major role in intestinal immunity, are portals of entry for significant pathogens, and may be important in Crohn's disease. Whereas their microscopic anatomy and immune function are well described, surprisingly little is known of their macroscopic anatomy and distribution. Our aim was to assess their number, area, and distribution in the normal distal ileum, with particular reference to patient age. METHODS: Distal ilea (200 cm) obtained at autopsy from 55 adults without intestinal disease were opened along the mesenteric border, fixed in acetic acid, and transilluminated. Peyer's patches were counted, and the length, breadth, and distance from the ileocecal valve were recorded. RESULTS: Patches were most numerous in the terminal 10-15 cm where they formed a lymphoid ring. More proximal patches were oval, antimesenteric, and irregularly spaced. By area, 46% of patch tissue occurred in the terminal 25 cm. The mean number of patches ranged from 29.4 +/- 5.4 in the youngest group studied, to 19.0 +/- 3.0 in the oldest. Total patch area was greatest in the group aged 21-30 (47.4 +/- 1.0 cm2). CONCLUSION: Peyer's patches are concentrated in the distal 25 cm of ileum but extend proximally for 200 cm. The variation in their size, shape, and distribution in different individuals is greater than often appreciated and may influence the presentation of diseases centered on these structures.