Approach Considerations
The most helpful laboratory studies include the following:
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Electrolyte, creatinine, and blood urea nitrogen (BUN) levels
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Complete blood count (CBC)
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Urinalysis
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Urine culture
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Lupus serologies
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Measurement of complement components (ie, C3, C4)
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Antistreptolysin-O (ASO) titer
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Anti-DNAase B
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Perinuclear antineutrophil cytoplasmic antibody (P-ANCA) measurement
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Cellular antineutrophil cytoplasmic antibody (C-ANCA) assessment
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Serum IgA measurement [1]
If the child has a history consistent with acute poststreptococcal glomerulonephritis (GN), such as low C3, positive ASO, and anti-DNAase B, a provisional diagnosis of this disorder can be made. Supportive care and observation for improvement within 10-14 days is reasonable. If a diagnosis of acute poststreptococcal GN seems unlikely, a percutaneous renal biopsy is the single most effective mechanism to arrive at a pathologic diagnosis.
Laboratory findings in tubulointerstitial nephritis (TIN) include hematuria, eosinophilia, sterile pyuria, low-grade proteinuria, eosinophiluria, and urinary white blood cell casts. A percutaneous renal biopsy is the criterion standard for diagnosing TIN. With TIN, the hallmarks of GN (ie, edema, hypertension, sodium chloride retention) are not present. Tubular dysfunction is the predominant feature.
The pattern of tubular dysfunction that develops in TIN depends on the tubular segment(s) involved. Proximal tubular lesions result in aminoaciduria, glucosuria, phosphaturia, uricosuria, beta2 microglobinuria, and bicarbonaturia, often producing proximal renal tubular acidosis. [8] Lesions involving the distal tubule result in an inability to acidify urine (distal renal tubular acidosis), to regulate sodium balance, and to secrete potassium. Lesions affecting the medulla and papilla result in an inability to concentrate urine.
These tubular functions may be tested by calculating the fractional excretion of phosphate or bicarbonate, measuring the urinary glucose excretion, and measuring the urine pH and osmolality with fasting.
Imaging studies
Renal ultrasonography is usually performed to exclude other causes of hypertension and hematuria, such as renal artery stenosis (ie, small, abnormal kidney on one side), anatomic abnormalities, a tumor, and stones. The kidneys are frequently echodense when GN is present. The kidneys may be abnormally large or small.
No imaging tests are sensitive or specific for TIN. Renal ultrasonography may show large kidneys with normal echogenicity.
Renal biopsy
If a specific diagnosis is needed for a child with hematuria, proteinuria, edema, and hypertension (ie, nephritis), a percutaneous renal biopsy usually is the criterion standard for identifying a specific pathology. Kidney biopsy findings are diagnostic for TIN.
Histologic Findings
In glomerulonephritis (GN), light microscopy usually reveals infiltration of the kidney by lymphocytes, polymorphonuclear leukocytes, or both. Immunofluorescence microscopy may reveal IgG, IgA, IgM, or complement in mesangial or vascular distribution, depending on the type of GN. Electron microscopy may reveal deposits in mesangial, subendothelial, or subepithelial tissue or in a combination of tissues, depending on the type of GN present. Replacement of renal tissue by scar tissue (tubular atrophy and interstitial fibrosis) is the final common pathway for several types of GN.
For tubulointerstitial nephritis (TIN), light microscopy reveals focal interstitial infiltrates of edema that contain lymphocytes and eosinophils. Tubular injury is usually greater than glomerular or vascular injury.
