Hematuria (Case 16)
Spirithoula Vasilopoulos MD and Michael Gitman MD
Case: The patient is a 60-year-old male who, during an annual physician visit, was found to have hematuria. His medical history is significant for emphysema from years of smoking, as well as an episode of right-sided nephrolithiasis approximately 1 year ago. At that time he passed the stone spontaneously, and subsequently his urinalysis had been normal. His medications include albuterol and ibuprofen. After hearing of the hematuria, he states that he has never seen any blood in his urine and he certainly does not have any pain. Other than complaints of his chronically poor urinary stream, he feels great. After some discussion, he agrees to complete any evaluation that is necessary.
Differential Diagnosis
Speaking Intelligently
Hematuria is a common clinical problem, occurring in 10% to 20% of adult men and postmenopausal women. It can originate from anywhere within the genitourinary tract including the kidneys, ureters, bladder, and urethra. Its clinical significance varies dramatically from innocuous diseases such as cystitis to a life-altering diagnosis, such as renal failure or malignancy. A thorough history, physical exam, and urine evaluation will help to identify the cause of hematuria and the extent of clinical evaluation that is necessary.
• Determine the context in which the sample was taken. A urinalysis done in the setting of urinary tract infection (UTI), catheter trauma, significant coagulopathy, menstruation, after sexual intercourse, or after vigorous exercise may need to be repeated.
• If the hematuria is evaluated in the appropriate setting, determine whether the red blood cells originated in the kidney or in the lower urinary tract.
• Red blood cells originating in the kidney will be dysmorphic, while red blood cells that originate in the lower urinary tract will retain their usual morphology on visual exam. If the red blood cells originated in the glomerulus, you may see red blood cell casts.
• Hematuria accompanied by proteinuria is often of glomerular origin.
• Categorize the hematuria as gross or microscopic, and glomerular or nonglomerular. Deciding on the origin will help narrow the differential and assist in ordering the appropriate diagnostic tests and referring the patient to the appropriate specialist.
• Determine the degree of hematuria: Is it microscopic or macroscopic? Although macroscopic hematuria can be seen with glomerular diseases, it is much more often a sign of lower urinary tract pathology and is often the initial symptom of genitourinary cancer.
• Look for associated symptoms, which are extremely important. Unintentional weight loss, fevers of unclear origin, or night sweats suggest neoplasm. Colicky flank pain radiating to the groin associated with nausea or vomiting suggests nephrolithiasis. Difficulty initiating urination, poor urinary stream, and nocturia suggest benign prostatic hypertrophy (BPH). Dysuria, frequency, urgency, and suprapubic pain suggest cystitis.
• Ask about recent skin infections or URIs, and the timing of the infections relative to the onset of hematuria. Post-streptococcal glomerulonephritis occurs over a week after an infection, whereas hematuria from IgA nephropathy can be seen concurrent with the URI.
• A family history of males with kidney disease and hearing deficit suggests Alport syndrome, whereas a family history of renal failure and stroke suggests polycystic kidney disease.
• Review cigarette smoking history and toxin exposures. Exposure to aromatic amines, aniline dyes, benzidine, or cyclophosphamide, as well as analgesic abuse, are risk factors for urothelial carcinoma.
• Hypertension and edema are common in glomerular diseases, but they are not specific findings. Large, polycystic kidneys can often be palpated during the abdominal exam.
• Suprapubic tenderness can be seen with cystitis.
• Costovertebral tenderness can be seen with pyelonephritis or nephrolithiasis.
• Prostatic enlargement and tenderness can be seen with BPH or prostatitis.
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IgA Nephropathy
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IgA nephropathy is caused by the production of abnormal immunoglobulin A molecules that cannot be effectively cleared from the circulation. These IgA complexes deposit in the mesangial portion of the glomeruli and cause an inflammatory reaction that leads to renal damage. It is usually a slowly progressive disease, but more than 25% of those affected will eventually progress to end-stage renal disease.
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