Hematuria is classified into microscopic hematuria and macroscopic hematuria. Microscopic hematuria is defined as a normal appearance of urine in which more than 3 red blood cells are observed per high-power field under the microscope. Macroscopic hematuria refers to urine that appears red or brown, sometimes mixed with blood clots; the presence of 1 ml of blood per liter of urine can cause macroscopic hematuria.
When urine color is abnormal, the following conditions should be excluded: (1) Food influence: beetroot, red dragon fruit, food coloring. (2) Drug influence: deferoxamine, rifampicin, etc. (3) Exercise, fever, menstruation in women, trauma, etc.
Characteristics of renal hematuria:
(1) Hematuria throughout the entire urinary process; if the lesion is in the urethra, initial hematuria can be seen; if the lesion is in the bladder trigone, terminal hematuria can be observed.
(2) Non-coagulating (within the kidney, endothelial cells, epithelial cells, and renal tubular epithelial cells secrete fibrinolytic protease activator urokinase, which can cause anticoagulation[1]).
(3) Painless hematuria; if symptoms such as dysuria, lumbar pain, or lower abdominal pain occur, urinary tract infection or stones are suggested.
(4) Presence of red blood cell casts; casts are formed by mucoprotein secreted by the epithelial cells lining the nephron loop, distal tubule, and collecting duct. Therefore, the occurrence of red blood cell casts indicates renal-origin hematuria.
(5) Red blood cell morphology analysis shows more than 70% dysmorphic red blood cells, mainly acanthocytes and burr cell-like forms. Major causes include mechanical damage when cells pass through the gaps in the glomerular basement membrane, and some red blood cells are damaged in the hypotonic environment of the tubule, releasing hemolytic substances that affect membrane deformation of other red blood cells in the renal microenvironment[2].
(6) Accompanied by proteinuria, hypertension, edema, and other manifestations of kidney disease.
References:
[1] Zhuang Yongze, Xie Fuan. Fibrinolytic activators and their inhibitors and kidney diseases [J]. Foreign Medicine Urology System Branch, 2001, 21(04):158-161.
[2] Schramek P, Moritsch A, Haschkowitz H, Binder BR, Maier M. In vitro generation of dysmorphic erythrocytes. Kidney Int. 1989 Jul;36(1):72-7.
Additionally, patients should be asked the following questions:
(1) Whether there was intense activity, trauma, or fever leading to transient bleeding.
(2) Whether there is frequent urination, urgency, or dysuria to exclude urinary tract infection.
(3) Whether there is difficulty in urination, incomplete urination sensation, or urinary leakage, to exclude benign prostatic hyperplasia, prostate tumors, or bladder tumors (risk factors include age >35 years, smoking, occupational exposure to pigments, macroscopic hematuria, chronic cystitis or bladder irritative symptoms, history of pelvic radiotherapy, history of analgesic abuse, cyclophosphamide use).
(4) Whether there is upper respiratory infection or intestinal infection to exclude IgA mucosal immune disease.
(5) Whether there is a family history of kidney disease, presence or absence of Alport syndrome (hematuria, progressive renal function decline, sensorineural hearing loss), polycystic kidney disease, sickle cell anemia, etc.
(6) Whether the patient is taking warfarin or has hemorrhagic diseases.
(7) Whether non-steroidal anti-inflammatory drugs (NSAIDs) are used.
(8) Whether there is a history of tuberculosis.
Physical examination includes:
(1) Petechiae on skin and mucous membranes.
(2) Hearing evaluation.
(3) Abdominal physical examination: renal artery bruit, renal percussion tenderness, ureteral point tenderness, palpation of bladder and kidneys.
(4) Lower limb edema.
(5) Blood pressure measurement.
