2025 – PAGE 383 – NEPHROLOGY

INTRINSIC RENAL DISEASE

RENAL FAILURE

Obviously, creatinine goes up in renal failure since it’s still being made but not excreted. If the patient is still making some urine, the urine sodium will be HIGH (> 25) due to renal salt wasting from dysfunctional tubules. Also, there is eventually decreased urine output, and the resulting increased total body water leads to a decreased drive for the kidneys to retain sodium. When there’s decreased urine output, a patient who drinks water beyond the insensible losses will become hyponatremic.

PEARLS: Symptoms of renal failure may include FTT, a normocytic anemia due to decreased erythropoietin production, hypertension, vitamin D deficiency (and thus hypocalcemia and elevated phosphorus), secondary hyperparathyroidism due to hypocalcemia, neurologic changes from uremia and metabolic acidosis from bicarb losses and decreased acid excretion.

PEARLS: For patients with end-stage renal failure (ESRD), always keep strict ins/outs, replace the measured urine output cc for cc with D5 0.2 NS, and give an additional 1/3 of the calculated daily fluid requirement by weight (the latter is for insensible losses). Use a low sodium solution (D5 0.2 NS) because the total body sodium is normal and this is truly for maintenance fluid/water only.

PEARLS: Fractional Excretion of Sodium = How much Na+ is EXCRETED as compared to reabsorbed. So a HIGH FeNa generally means a relatively HIGH amount of Na+ being excreted into the urine! The formula can be written in many ways. For some reason, I remember YOU NACR! PEE NACR! FeNa+ = [(UNa/UCr) / (PNa/PCr)]. Division only, no multiplication. Calculating a FeNa can be useful in acute renal failure with low urine output. A FeNa of < 1% suggests prerenal disease with low renal perfusion. The kidneys are working to resorb sodium and retain volume. A FeNa > 2% suggests tubular or glomerular damage.

OLIGURIA

A child with acute tubular necrosis and oliguria (voiding < 300–500 cc/day) has a poor prognosis.

RENOVASCULAR DISEASE

If given the history of a female teen with new-onset hypertension, FIBROMUSCULAR DYSPLASIA (a type of renovascular disease) is likely the diagnosis. She likely has RENAL ARTERY STENOSIS (RAS). Never give an ACE inhibitor to a patient with RAS, since the drug can interfere with autoregulation of glomerular pressure and lead to kidney damage and failure.

ACUTE INTERSTITIAL NEPHRITIS

Acute interstitial nephritis is inflammation of the kidney interstitium, often triggered by medications, infections, or autoimmune diseases. Elevated serum creatinine typically prompts an investigation. If present, symptoms may include fever, rash, arthralgias, and flank pain. The diagnosis is supported by eosinophilia, pyuria, WBC casts, and eosinophils in urine. A renal biopsy with interstitial inflammation and edema confirms the diagnosis definitively but may not be needed if symptoms are induced by a drug and improve once the drug is stopped. Treat by discontinuing the offending agent and using corticosteroids in severe cases.