Background An early posttransplant biomarker/surrogate marker for kidney allograft loss has the potential to guide targeted interventions. Previously published findings, including results from the Clinical Trials in Organ Transplantation (CTOT)-01 study, showed that elevated urinary chemokine CXCL9 levels and elevated frequencies of donor-reactive interferon gamma-(IFNγ)-producing T cells by enzyme linked immunosorbent spot (ELISPOT) assay associated with acute cellular rejection within the first year and with lower 1-year posttransplant estimated glomerular filtration rate (eGFR). How well these biomarkers correlate with late outcomes, including graft loss, is unclear. Methods In CTOT-17, we obtained 5-year outcomes in the CTOT-01 cohort and correlated them with a) biomarker results and b) changes in eGFR (Chronic Kidney Disease Epidemiology Collaboration formula) over the initial 2 years posttransplant using univariable analysis and multivariable logistic regression. Results Graft loss occurred in 14/184 subjects (7.6%) 2 to 5 years posttransplant. Neither IFNγ ELISPOTs nor urinary CXCL9 were informative. In contrast, a ≥40% decline in eGFR from 6 months to 2 years posttransplant independently correlated with thirteen-fold odds of 5-year graft loss [adjusted odds ratio (aOR) 13.1; 95% CI 3.0–56.6], a result that was validated in the independent Genomics of Chronic Allograft Rejection cohort (n=165, aOR: 11.2). Conclusions We conclude that while pre and early posttransplant ELISPOT and chemokine measurements associate with outcomes within 2-years posttransplant, changes in eGFR between 3 months or 6 months and 24 months are better surrogates for 5-year outcomes, including graft loss.

Simultaneous liver‐kidney allocation protocols allocate dual organs based on a sustained eGFR of 30 mL/min or less. A 2017‐UNOS update includes CKD3 as dual organ candidates but only when the listing eGFR is <30 mL/min while recommending a "safety net" for prioritized kidney listing post‐LT. We retrospectively reviewed adult LTs examine whether the UNOS proposal captured the LT population at highest risk for developing post‐LT ESRD. Among 290 LT recipients, 67 had pre‐LT CKD3, 141 had AKI, of whom 47 required dialysis (<4 weeks). During follow‐up, 25 (8.62%) developed ESRD, while 70 (24.1%) died. In adjusted Cox models, CKD3 had an independent association with post‐LT ESRD (adjusted HR 4.8; P = 0.001), independent of AKI. Interestingly, CKD3 with listing GFR >30 mL/min was still significantly associated with post‐LT ESRD. AKI was associated with reduced post‐LT survival (adjusted HR 1.9; P = 0.02), albeit only in the first‐year post‐LT. Severe AKI‐D was associated with post‐LT ESRD and mortality. The safety net would have captured only 60% of all post‐LT ESRD cases in our cohort. Pre‐LT CKD3 was associated with increased risk of post‐LT ESRD above the recommended cutoff for listing GFR. These findings, if generalizable in larger cohorts have important implications for dual organ allocation.

Patients with chronic kidney disease (CKD) are three times more likely to have myocardial infarction (MI) and suffer from increased morbidity and higher mortality. Traditional and unique risk factors are prevalent and constitute challenges for the standard of care. However, CKD patients have been largely excluded from clinical trials and little evidence is available to guide evidence-based treatment of coronary artery disease in patients with CKD. Our objective was to assess whether a difference exists in the management of MI (ST-segment elevation myocardial infarction and non-ST-segment elevation myocardial infarction) among patients with normal kidney function, CKD stage III–V, and end-stage renal disease (ESRD) patients. We conducted a retrospective cohort study on patients admitted to Staten Island University Hospital for the diagnosis of MI between January 2005 and December 2012. Patients were assigned to one of three groups according to their kidney function: Data collected on the medical management and the use of statins, platelet inhibitors, beta-blockers, and angiotensin converting enzyme inhibitors/angiotensin receptor blockers were compared among the three cohorts, as well as medical interventions including: catheterization and coronary artery bypass graft (CABG) when indicated. Chi-square test was used to compare the proportions between nominal variables. Binary logistic analysis was used in order to determine associations between treatment modalities and comorbidities, and to account for possible confounding factors. Three hundred and thirty-four patients (mean age 67.2±13.9 years) were included. In terms of management, medical treatment was not different among the three groups. However, cardiac catheterization was performed less in ESRD when compared with no CKD and CKD stage III–V (45.6% vs 74% and 93.9%) ( P <0.001). CABG was performed in comparable proportions in the three groups and CABG was not associated with the degree of CKD ( P =0.078) in binary logistics regression. Cardiac catheterization on the other hand carried the strongest association among all studied variables ( P <0.001). This association was maintained after adjusting for other comorbidities. The length of stay for the three cohorts (non-CKD, CKD stage III–V, and ESRD on hemodialysis) was 16, 17, and 15 days, respectively and was not statistically different. Many observations have reported discrimination of care for patients with CKD considered suboptimal candidates for aggressive management of their cardiac disease. In our study, medical therapy was achieved at high percentage and was comparable among groups of different kidney function. However, kidney disease seems to affect the management of patients with acute MI; percutaneous coronary angiography is not uniformly performed in patients with CKD and ESRD when compared with patients with normal kidney function.

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Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is the most common electrolyte disorder associated with neurological conditions. Parkinson's disease (PD) has not been known to be causative of SIADH. We present the case of a 71-year-old male patient with diabetes type II (T2DM) and hypothyroidism admitted with progressive confusion, slow speech, and severe fatigue for one week, accompanied by sluggish body movements for a few months. A neurological exam revealed mild arm rigidity, bradykinesia, resting tremors, and stiff gait. The exam was otherwise normal. Initial blood work showed hypo-osmolar hyponatremia (Na 122 mEq/L, serum osmolarity (Osm) 275 mOsm/kg, and urine Osm 672 mOsm/Kg). CT chest showed localized infiltrate. The initial diagnosis was SIADH secondary to pulmonary process, most probably pneumonia. After starting him on a fluid restriction of 1.5 L/day and urea 15 mg BID, sodium improved gradually to 133 mEq/L on discharge. Urine osmolality continued to be elevated ranging between 700 and 800 mOsm/Kg. An active pulmonary process was ruled out by a pulmonologist. Parkinsonism was diagnosed four weeks after discharge by Neurology who started carbidopa/levodopa. As extrapyramidal symptoms improved, urine osmolality improved as well to 400 mOsm/Kg. Sodium level was maintained between 135 and 137 while urea treatment was stopped and fluid restrictions removed. New-onset SIADH was thought to be secondary to Parkinson's disease. Parkinson's disease treatment (carbidopa/levodopa) is known to cause SIADH. In this case, the treatment itself and a dose increase led to improvement in sodium levels and urine osmolality concomitantly with the improvement of the patient's extrapyramidal symptoms.