MY APPROACH to Chronic Kidney Disease
A 56-year-old male is admitted to the Family Medicine service with community-acquired pneumonia. He has a 4-year history of hypertension treated with enalapril/HCTZ daily. His blood pressure is 136/82, pulse is 94, temperature is 38.5oC, and O2 saturation is 93% on room air. His jugular venous pressure is 5 cm, and he has signs of consolidation in the left lower lobe. There is no edema. Initial laboratory studies show a white blood cell count of 14,200, hemoglobin of 13.1 grams, and normal platelet count. His sodium level is 142 mEq/L, potassium is 3.8 mEq/L, HCO3 is 24 mEq/L, BUN is 38 mg/dl, and creatinine is 2.4 mg/dl. The creatinine 1 year ago was 1.8 mg/dl. The serum phosphorus is 4.2.
His calculated GFR by serum creatinine is 40 ml/min (stage 3 chronic kidney disease; CKD).
In general, one could approach this patient with CKD in a way that is analogous to preventive medicine—primary, secondary, and tertiary levels of prevention.
Primary: Identify whether the renal insufficiency is acute (reversible) or chronic. Acute renal failure is supported by lack of anemia, normal phosphate levels and normal renal size, while chronic renal disease may be associated with normocytic anemia, hyperphosphatemia, or small, “shrunken” kidneys due to fibrosis. Obviously, if previous determinations of renal function are available one can better determine chronicity. Second, is a treatable entity present? Examples may include pre-renal azotemia, obstruction, renal vascular disease, or some forms of glomerulonephritis. One would wish to evaluate volume status—this patient has a normal blood pressure and no evidence of congestive heart failure or volume depletion. Renal vascular disease can be assessed by examination for carotid, abdominal, or femoral bruits, as ASCVD is the predominant cause of renal vascular disease, particularly in this age group. A urinalysis and sediment exam for casts, hematuria, and proteinuria can be used to determine the possibility of glomerulonephritis. Finally, a renal ultrasound can assess renal size and exclude obstructive uropathy.
Secondary: Each chronic kidney abnormality tends to progress at a consistent rate. Some, such as diabetes, progress at a relatively rapid rate once the GFR begins to decline (interval- to end-stage renal disease averages 3 to 5 years from onset of stage 2 CKD). Diseases such as chronic pyelonephritis and hypertensive nephrosclerosis progress much slower (duration in excess of 10 to 15 years). Others may be highly variable, such as IgA nephropathy. Once the GFR is significantly reduced (<30 ml/min), renal function may decline even if the underlying etiology is corrected. However, there are many examples in which the renal function has remained stable even with the GFR <15 ml/min. In order to slow the rate of progression, one would attempt to treat the underlying etiology, if feasible, and attempt to slow any potential endogenous progression. A number of interventions to slow endogenous progression have been utilized, including protein restriction, blood pressure control, inhibition of the renin-angiotensin-aldosterone axis, and phosphorus control. Of these, blood pressure control has most convincingly been shown to be beneficial with a goal of blood pressure <130/80, if feasible. This can include inhibition of the renin-angiotensin-aldosterone axis, but it is controversial that inhibition has any additional benefit other than blood pressure control. Protein restriction has not been shown to be significantly helpful, but one would wish to avoid excessive protein intake (>1.2 g/kg/day). Phosphorus control (serum phosphorus <4.5 mg/dl) slows the rate of progression and maintains normal PTH levels. The latter is accomplished with phosphorus restriction and use of phosphate binders.
Tertiary: Treatment of associated or comorbid conditions: This would, of course, include management of acid–base homeostasis, electrolyte abnormalities, volume status, and anemia. One expects a hyperchloremic metabolic acidosis with stage 3 and 4 CKD due to decreased ammoniagenesis and ammonium excretion, while a mild anion gap acidosis may occur with stage 5 CKD. The goal is to maintain a bicarbonate level >20 mEq/L. This can usually be accomplished with oral bicarbonate equivalent of 0.4 to 0.6 mEq/kg/day. Hyperkalemia is avoided by restricting potassium intake to 60 mEq/day. One expects volume retention with CKD, which is usually controlled with sodium restriction (2000 mg/day) and furosemide 20 to 160 mg orally twice daily. Use of erythrocyte-stimulating agents is best left to the nephrologist. Finally, accelerated atherosclerosis is present with CKD and is multifactorial, including hypertension, dyslipidemia, and increased homocysteine levels. The increased homocysteine levels are virtually impossible to fully correct but can be reduced with folate supplementation at 1 to 2 mg daily.
Click on any of these tags to subscribe to Topic Alerts. Once subscribed, you can get a single, daily email any time PracticeUpdate publishes content on the topics that interest you.
Visit your Preferences and Settings section to Manage All Topic Alerts