Diabetic kidney disease (DKD) is a significant contributor to kidney failure, particularly in Singapore.
A recent study conducted by scientists at Duke-NUS Medical School and elsewhere has shed light on the metabolic abnormalities that drive progressive kidney injury in DKD. The findings may offer better ways to detect the risk of kidney failure.
The Scope of Diabetic Kidney Disease
In Singapore, DKD is a leading cause of kidney failure, with approximately nine people diagnosed with kidney failure daily. Up to 40% of individuals with long-standing diabetes eventually develop kidney disease.
The study is part of the Diabetes Study in Nephropathy and other Microvascular Complications (DYNAMO), a global collaborative effort involving clinicians and scientists from six countries and 25 institutions.
The overarching goal of DYNAMO is to reduce the prevalence of DKD. The research team conducted experiments on a preclinical model and analyzed clinical data and samples from a Singaporean cohort of 230 patients with type 2 diabetes.
The Key Findings
The study identified metabolic abnormalities leading to an accumulation of lactate, a byproduct of cellular energy production. This accumulation appeared to result from impaired mitochondrial function in kidney tubule cells.
Elevated lactate levels were closely linked to albumin in urine, which serves as a marker of kidney damage. This suggests that lactate may signal distress due to high protein levels in urine.
Treatment with angiotensin receptor blockers (ARBs), a common therapy for DKD, reversed the metabolic abnormalities and prevented kidney injury in the preclinical model.
Among the patients, those with the highest urinary lactate levels faced a significantly increased risk of eventual kidney failure.
The Implications
Monitoring urinary lactate could potentially help predict prognosis and guide the management of diabetic kidney disease. The findings highlight the importance of optimizing kidney energy metabolism to slow disease progression.
The researchers plan to conduct follow-up studies to investigate whether lactate itself may cause kidney injury. If successful, this line of research could lead to innovative therapeutic approaches for preventing DKD by reducing kidney lactate generation or blocking its effects.
This study provides valuable insights into the mechanisms driving progressive kidney disease in diabetes.
It demonstrates the potential for precision interventions that target the underlying drivers of the disease, with the hope of developing innovative prevention strategies in the future.
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The research findings can be found in Kidney International.
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