Renal Function and All-Cause Mortality Risk Among Cancer Patients

Abstract

Renal dysfunction predicts all-cause mortality in general population. However, the prevalence of renal insufficiency and its relationship with mortality in cancer patients are unclear.We retrospectively studied 9465 patients with newly diagnosed cancer from January 2010 to December 2010. Renal insufficiency was defined as an estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2 using the Chronic Kidney Disease Epidemiology Collaboration equation. The hazard ratio (HR) of all-cause mortality associated with baseline eGFR was assessed by Cox regression.Three thousand sixty-nine patients (32.4%) exhibited eGFR <90 mL/min/1.73 m2 and 3% had abnormal serum creatinine levels at the time of diagnosis. Over a median follow-up of 40.5 months, 2705 patients (28.6%) died. Compared with the reference group (eGFR ≥ 60 mL/min/1.73 m2), an elevated all-cause mortality was observed among patients with eGFR < 60 mL/min/1.73 m2 stratified by cancer stage in the entire cohort, the corresponding hazard ratios were 1.87 (95% CI, 1.41–2.47) and 1.28 (95% CI, 1.01–1.62) for stage I to III and stage IV, respectively. However, this relationship was not observed after multivariate adjustment. Subgroup analysis found that eGFR < 60 mL/min/1.73 m2 independently predicted death among patients with hematologic (adjusted HR 2.93, 95% CI [1.36–6.31]) and gynecological cancer (adjusted HR 2.82, 95% CI [1.19–6.70]), but not in those with other cancer. Five hundred fifty-seven patients (6%) had proteinuria. When controlled for potential confounding factors, proteinuria was a risk factor for all-cause mortality among patients in the entire cohort, regardless of cancer stage and eGFR values. When patients were categorized by specific cancer type, the risk of all-cause death was only significant in patients with digestive system cancer (adjusted HR, 1.85 [1.48–2.32]).The prevalence of renal dysfunction was common in patients with newly diagnosed cancer. Patients with eGFR < 60 mL/min/1.73 m2 or proteinuria were associated with increased risk for all-cause mortality, this relation depended on cancer site.

Preoperative chronic kidney disease predicts poor oncological outcomes after radical cystectomy in patients with muscle-invasive bladder cancer

“…The effect of CKD on the risk of poor prognosis with malignant disease is controversial. The presence of CKD was associated with an increased risk of death in cancer patients in several studies [ 33 , 34 ]. Na SY et al [ 33 ] retrospectively reviewed the cases of 8,223 cancer patients and reported that cancer-specific mortality was significantly higher in the patients with CKD than those without CKD (the adjusted HR: 1.12 for patients with an eGFR of 30-59 mL/min/1.73 m2, P = 0.04 and 1.75 for patients with an eGFR <30 mL/min/1.73 m2, P < 0.001).…”

“…CKD is not an independent risk factor for survival in patients with lung cancer [ 33 , 35 ] and breast cancer [ 33 , 36 ]. Currently, CKD is reported as an independent risk factor for survival in head and neck, stomach, liver, colorectal, urinary tract, gynecological and hematologic malignancy [ 33 , 34 ].…”

Risk-stratified surveillance protocol improves cost-effectiveness after radical nephroureterectomy in patients with upper tract urothelial carcinoma

“…The reason for the strong association between CKD and poor recurrence-free survival is not clear. Previous studies have suggested that kidney and urinary tract cancers are high risk for renal dysfunction due to tumor location (obstruction, and/or reduction of nephron mass) [16][17][18]. Our previous studies suggested that patients with stage 3 CKD had significantly higher risk for recurrence and cancer death compared to those without CKD [19][20][21].…”

Cisplatin induces acute kidney injury and pyroptosis in mice through the exosome miR-122/ELAVL1 regulatory axis

“…However, it usually causes AKI in these patients. Previous studies have found that renal insu ciency can independently predict a poor prognosis for cancer patients [29]. However, to date, the mechanism of cisplatin-induced AKI has not been studied in depth, and there is still no effective treatment.…”