Derivation and Validation of a Renal Risk Score for People With Type 2 Diabetes

OBJECTIVE

Diabetes has become the leading cause of end-stage renal disease (ESRD). Renal risk stratification could assist in earlier identification and targeted prevention. This study aimed to derive risk models to predict ESRD events in type 2 diabetes in primary care.

RESEARCH DESIGN AND METHODS

The nationwide derivation cohort included adults with type 2 diabetes from the New Zealand Diabetes Cohort Study initially assessed during 2000–2006 and followed until December 2010, excluding those with pre-existing ESRD. The outcome was fatal or nonfatal ESRD event (peritoneal dialysis or hemodialysis for ESRD, renal transplantation, or death from ESRD). Risk models were developed using Cox proportional hazards models, and their performance was assessed in a separate validation cohort.

RESULTS

The derivation cohort included 25,736 individuals followed for up to 11 years (180,497 person-years; 86% followed for ≥5 years). At baseline, mean age was 62 years, median diabetes duration 5 years, and median HbA_1c 7.2% (55 mmol/mol); 37% had albuminuria; and median estimated glomerular filtration rate (eGFR) was 77 mL/min/1.73 m². There were 637 ESRD events (2.5%) during follow-up. Models that included sex, ethnicity, age, diabetes duration, albuminuria, serum creatinine, systolic blood pressure, HbA_1c, smoking status, and previous cardiovascular disease status performed well with good discrimination and calibration in the derivation cohort and the validation cohort (n = 5,877) (C-statistics 0.89–0.92), improving predictive performance compared with previous models.

CONCLUSIONS

These 5-year renal risk models performed very well in two large primary care populations with type 2 diabetes. More accurate risk stratification could facilitate earlier intervention than using eGFR and/or albuminuria alone.Compared with people without diabetes and even after adjusting for other risk factors, those with type 2 diabetes have three to five times the risk of developing end-stage renal disease (ESRD) resulting in dialysis, renal transplantation, or early mortality (1). Diabetes has become the leading cause of ESRD in many countries (2), with certain ethnic groups having much higher rates than others (3,4). Apart from the large human cost of renal failure, there are significant national and individual economic costs for dialysis both for high- and low-income countries (5,6), with some estimating that 30% of the world’s $1.1 trillion in medical costs of dialysis over this decade will result from diabetic kidney disease (2,7).Early identification of those most likely to progress to ESRD among the diabetic population could prompt earlier optimization of preventive therapies in primary care or earlier referral to specialist care. There is evidence that tight control of glycemia (8,9) and blood pressure (BP) as well as use of ACE inhibitors and angiotensin II receptor blockers (ARBs) can reduce the rate of progression of diabetic kidney disease (10,11). While estimated glomerular filtration rate (eGFR) and the presence of albuminuria are used to assess renal deterioration, other clinical factors such as glycemia are also associated with risk of progression to ESRD (9,12,13). Renal risk stratification models already exist for those with advanced chronic kidney disease (CKD; stages 3–5) (14) or established diabetic nephropathy (15). However, these models may be more appropriate for use in secondary care than in primary care settings. While the QKidney models have been derived from a primary care population, these include diabetes only as a dichotomous variable and do not include glycemia, serum creatinine (sCr), eGFR, or albuminuria (1). Another renal risk equation has recently been published for those with type 2 diabetes without advanced disease from the ADVANCE clinical trial (16).We therefore aimed to derive and validate a model to predict 5-year risk of end-stage renal events, including dialysis, renal transplantation, or death from renal failure, among people with type 2 diabetes without advanced kidney disease within a primary care context and to compare the model’s performance with other risk assessments.     

Abnormal thyroid function predicts mortality in patients receiving long-term peritoneal dialysis: A case-controlled longitudinal study

BackgroundThe population of uremia patients receiving long-term peritoneal dialysis (PD) is growing, and abnormal thyroid function occurs increasingly in patients with chronic kidney disease in comparison with the normal population. We aimed to elucidate the clinical impact of abnormal thyroid function in long-term PD patients.MethodsThis was a retrospective, case-controlled, longitudinal study. We collected the characteristics, laboratory data, dialysis parameters, and thyroid and heart function of patients who underwent long-term PD for >8 years during the past 25 years in Taipei Veterans General Hospital, Taiwan. Patients with hyperthyroidism were excluded. None of these subjects presented a recent history of infection or inflammatory disease or took any drugs known to influence thyroid function. Abnormal thyroid function was defined as the presence of primary hypothyroidism and sick euthyroid syndrome.ResultsA total of 46 patients were enrolled. The mean duration of PD therapy was 147.8 (48.3) months. Nineteen of 46 (41.3%) patients had abnormal thyroid function tests. Patients with abnormal thyroid function had a worse prognosis in cumulative patient survival analysis by Kaplan–Meier method (p = 0.02). After adjusting for diabetes mellitus, cardiothoracic ratio, C-reactive protein (CRP), and cardiovascular diseases, abnormal thyroid function remained as an independent predictor of patient survival (hazard ratio = 7.633, 95% confidence interval 1.3–43.9, p = 0.02). The CRP levels were significantly inversely correlated with free thyroxine levels (r = –0.547; p = 0.01). The most common cause of death among the patients was sepsis (67.7%) rather than cardiovascular disease (20.0%).ConclusionPD patients with abnormal thyroid function had poor cumulative survival. Lower thyroid hormone level in PD patients was associated with high CRP levels. Physicians should be alert for the presence of abnormal thyroid function and proinflammatory status in long-term PD patients.     

Section 3. Adrenal: Laparoscopic bilateral adrenalectomy for Cushing’s syndrome due to ACTH-independent macronodular adrenocortical hyperplasia

We performed simultaneous bilateral laparoscopic total adrenalectomy in two patients with Cushing’s syndrome due to ACTH-independent macronodular adrenocortical hyperplasia (AIMAH). Preoperative serum cortisol in the patients was 29.5 and 53.2 μg/dl, respectively. The clinical symptoms of the latter patient were advanced, and respiration was labored with orthopnea. Laparoscopic adrenalectomies were performed transabdominally in the sequential lateral decubitus positions with extension of the lateral abdominal wall of the affected side. Three 12-mm and three 5-mm trocars were positioned, and two trocar sites in the midline were used on both sides. The flexible fiberscope was inserted through the umbilical port. The adrenal glands were large, fragile, and multinodular. The maximal diameters of the removed glands were 7.8 and 8.7 cm, respectively. In both patients, the adrenal glands were successfully removed without fragmentation. The operation times were 505 and 320 min, and the estimated blood loss was 150 and 5 ml, respectively. Neither intraoperative nor postoperative complications occurred, although the latter patient required muscle training before ambulation on postoperative day 42. The procedures resulted in marked clinical improvements. Compliance with the substitutive therapy remained excellent, and the patients expressed a very high degree of satisfaction with the laparoscopic adrenal surgery. The procedures of bilateral laparoscopic adrenalectomy were successful, and provided increased experience with the laparoscopic techniques.