Q) I have a patient with stage 3a chronic kidney disease (glomerular filtration rate, 45-60 mL/min/1.73 m 2). I have her on a statin and an ACE inhibitor. Is there anything else I can do to slow the progression of kidney disease?
For patients with stage 3a chronic kidney disease (CKD), ongoing evaluation of risk factors and management can impact the rate of disease progression. The cornerstones of CKD care include identification and treatment of the cause; management of hypertension, albuminuria, and diabetes (if applicable); reduction of cardiovascular (CV) risk; and correction of metabolic abnormalities. 5
When considering factors that can contribute to kidney injury, clinicians should consider possible pre-, intra-, and post-renal processes that could potentially cause injury.
Prerenal: Approximately 20% of cardiac output is directed to the kidneys. Reduced left ventricular function, diastolic dysfunction, and pulmonary hypertension can all contribute to a reduction in renal blood flow and subsequent kidney injury. 6
Intrarenal: Exploration of possible intra-renal processes begins with a thorough history of any familial disease, hematuria, stones, proteinuria, and exposure to nephrotoxins. The nephrotoxicity profile of all medications should be examined, and patients should be educated about products, particularly OTC medications (eg, NSAIDs, common cold preparations, and herbal or weight-loss products), that can be harmful to the kidneys. Patients should also be made aware of the risk for contrast-induced renal injury, especially when considering imaging or cardiac testing. Since diabetes is a leading cause of kidney disease, good diabetic control can reduce nephropathy and slow disease progression.
Postrenal: Benign prostatic hypertrophy, kidney stones, and neurogenic bladder can all cause injury. These warrant further evaluation and treatment.
CKD often worsens existing hypertension, which is an independent risk factor for kidney failure. 7 Goal blood pressure (BP) for all patients without significant albuminuria should be < 140/90 mm Hg; for those with urinary albumin ≥ 30 mg/24 h, the goal is < 130/80 mm Hg. 8 Choice of antihypertensive agents can be tailored to other comorbidities, but an ACE inhibitor or angiotensin receptor blocker should be considered firstline treatment. Nocturnal hypertension is common in patients with CKD and an independent marker of CV risk. By dosing antihypertensive medications at bedtime, the clinician supports CV risk reduction. 9
CKD is an independent risk factor for CV disease, thus risk factor modification should be aggressively pursued. Regardless of the cause of CKD, cigarette smoking has been associated with a more rapid decline in renal function. Patients should be counseled on the risks and offered interventions to assist in smoking cessation. 10 There is also emerging evidence that exercise likely benefits the vascular health of the kidneys and appears to slow the rate of kidney decline. 11,12 Overall, lifestyle interventions that help mitigate CV risk may directly benefit preservation of kidney function as well.
Metabolic abnormalities increase with CKD progression. Maintaining proper bone health through control of phosphate/acidosis and calcium equilibrium reduces morbidity as it relates to vascular and soft-tissue calcification. This can often be effectively managed through dietary modifications in early to moderate CKD. As the number of functioning nephrons decrease in CKD, so does the ability of the kidney to maintain proper acid/base balance. Persistent metabolic acidosis is related to CKD progression. Acid buffering with oral bicarbonate may be needed to achieve a goal CO 2 of 22 to 32 mEq/L. 8