A 70-year-old man is brought to the hospital by his son due to worsening fatigue. The son states that his father does not like seeing doctors and has not been to one in 20 years. The patient frequently eats at fast food restaurants and rarely eats vegetables and fresh fruit. He has no known medical conditions other than chronic, intermittent back pain for which he uses over-the-counter painkillers. Physical examination shows an S4 heart sound, strong apical impulse, and clear lung fields. Abdomen examination reveals no bruit or other abnormalities. Neurological examination is normal. Laboratory results are as follows: Urinalysis shows trace protein and bland sediment without casts. Ultrasonogram of the abdomen reveals bilateral small kidneys and no evidence of hydronephrosis. Which of the following best explains this patient's findings?

Question

A 70-year-old man is brought to the hospital by his son due to worsening fatigue.  The son states that his father does not like seeing doctors and has not been to one in 20 years.  The patient frequently eats at fast food restaurants and rarely eats vegetables and fresh fruit.  He has no known medical conditions other than chronic, intermittent back pain for which he uses over-the-counter painkillers.  Physical examination shows an S4 heart sound, strong apical impulse, and clear lung fields.  Abdomen examination reveals no bruit or other abnormalities.  Neurological examination is normal.  Laboratory results are as follows:  Urinalysis shows trace protein and bland sediment without casts.  Ultrasonogram of the abdomen reveals bilateral small kidneys and no evidence of hydronephrosis.  Which of the following best explains this patient's findings?

Quizplus · Accepted Answer

Explanation: This patient with no medical care in years now has renal disease with elevated creatinine, bilateral small kidneys, bland urinalysis, trace proteinuria, and examination findings suggestive of chronic hypertension (eg, S4, strong apical impulse). This presentation is most consistent with hypertensive nephrosclerosis (HN). In response to chronic hypertension, renal arterioles undergo medial hypertrophy and intimal fibrosis, and subsequent endothelial damage leads to plasma protein and basement membrane material deposition into arteriolar walls (hyaline arteriolosclerosis). The resultant luminal narrowing causes a progressive decrease in renal blood flow, leading to glomerular ischemia with glomerular and tubular fibrosis and atrophy (glomerulosclerosis). These changes explain the characteristic findings: Elevated creatinine (decreased glomerular filtration rate) Ultrasonographically small, atrophic kidneys Bland (ie, no white/red blood cells) urinalysis with mild proteinuria (<1 g/day). Over time, azotemia, anemia (decreased renal erythropoeitin production), and other chronic kidney disease (CKD) manifestations (eg, fatigue) develop. Diagnosis is typically inferred in patients who have consistent findings (with no other obvious etiology) and a long history of uncontrolled hypertension (eg, no medical care in years, fast-food diet, suggestive physical examination findings). Biopsy is usually unnecessary. Most patients with hypertension will not develop renal insufficiency; risk seems increased in patients who have diabetes mellitus, have severe hypertension, or are African American (possibly related to APOL1 variants). Azotemia is typically slowly progressive (over years) and irreversible. This contrasts with bilateral renal artery stenosis, which may present similarly to HN (though typically with more rapid renal deterioration) but often improves with treatment (eg, angioplasty, stenting). (Choice A) Acute tubular necrosis typically results from ischemic (eg, hypotension) or toxic (eg, aminoglycoside, radiocontrast) insult, and urinalysis demonstrates muddy-brown casts. In addition, acute kidney injury (AKI) often causes edema or oliguria. (Choice B) Amyloidosis can cause CKD but is associated with nephrotic-range (>3.5 g/day) proteinuria and edema as well as enlarged kidneys with increased sonographic echogenicity (amyloid infiltration). (Choice C) Glomerulonephritis, an inflammatory process, would result in hematuria and red blood cell casts on urinalysis. (Choice E) Interstitial nephritis presents with AKI related to medications (eg, nonsteroidal anti-inflammatory drugs for back pain). Urinalysis often demonstrates pyuria and white blood cell casts, and the classic triad is fever, rash, and oliguria. (Choice F) Urinary obstruction (eg, benign prostatic hyperplasia) can cause AKI or CKD but is typically associated with a distended bladder or hydronephrosis. Educational objective: Hypertensive nephrosclerosis develops in patients with chronically uncontrolled hypertension and is characterized by hyaline arteriolosclerosis and ischemic glomerulosclerosis. Clinical features include progressive, irreversible renal insufficiency with mild proteinuria and small, atrophic kidneys.

A 70-Year-Old Man Is Brought to the Hospital by His