Introduction
Physical analytic methods
What information from stone analysis could be clinically relevant?
Morphological type | Subtype | Main components | Common causes |
---|---|---|---|
I | Ia | Whewellite | Dietary hyperoxaluria |
Ib | Whewellite | Stasis, low diuresis | |
Ic | Whewellite | Primary hyperoxaluria type I | |
Id | Whewellite | Malformative uropathy, stasis and confined multiple stones | |
Ie | Whewellite | Enteric hyperoxaluria | |
II | IIa | Weddellite | Hypercalciuria |
IIb | Weddellite ± whewellite | Hypercalciuria ± hyperoxaluria ± hypocitraturia | |
IIc | Weddellite | Hypercalciuria, stasis and confined multiple stones | |
III | IIIa | Uric acids | Low urine pH and stasis |
IIIb | Uric acids | Metabolic syndrome, diabetes | |
IIIc | Various urates | Hyperuricosuria and alkaline urine, UTI | |
IIId | Ammonium urate | Hyperuricosuria and diarrhea | |
IV | IVa1 | Carbapatite | Hypercalciuria, UTI |
IVa2 | Carbapatite | Distal renal tubular acidosis | |
IVb | Carbapatite | UTI, hypercalciuria. Etiology depends on minor components identified in the stone | |
IVc | Struvite | UTI by urease-splitting bacteria | |
IVd | Brushite | Hypercalciuria, PHPT, phosphate leak | |
V | Va | Cystine | Cystinuria |
Vb | Cystine | Cystinuria + inadequate therapy | |
VI | VIa | Proteins | Chronic pyelonephritis |
VIb | Proteins | Proteinuria, drugs, clots | |
VIc | Proteins | ESRF and excessive calcium + vitamin D supplementation |
Main associations | ||
---|---|---|
Ia or Ib + IIa or IIb | Whewellite + weddellite | Intermittent hyperoxaluria and hypercalciuria (dietary origin) |
Ia + IVa1 | Whewellite + carbapatite | Randall’s plaque, medullary sponge kidney |
IIa or IIb + IVa1 | Weddellite + carbapatite | Absorptive or resorptive hypercalciuria |
Ia or Ib + IIa or IIb + IVa or IVb | Whewellite + weddellite + carbapatite | Hyperoxaluria + hypercalciuria, medullary sponge kidney |
Ia + IIIb | Whewellite + uric acid | Hyperoxaluria + metabolic syndrome |
Keys for interpretation of stone analysis
Qualitative aspects
Quantitative data
Calcium oxalate
Calcium phosphate
The significant contribution of the stone morphology
COM stones
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Mild intermittent hyperoxaluria related to high oxalate intake
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Low diuresis with increased concentration of oxalate ions in urine
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Heavy hyperoxaluria either related to inherited diseases (primary hyperoxaluria type 1) or to enteric hyperoxaluria (ileal resection, bariatric surgery or chronic pancreatitis).
COD stones
Uric acid and urate stones
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Permanent low urine pH in the case of metabolic syndrome or type 2 diabetes mellitus, or in the case of intestinal alkali loss in patients having chronic hydro-electrolytic diarrhea (ileostomy, colectomy, hemorrhagic rectocolitis,…)
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High excretion of uric acid as observed in diabetes mellitus, in myelo- or lymphoproliferative syndromes or the case of Vaquez disease or rare cases of tubular dysfunction inducing a defect in urate reabsorption. Of note, among patients suffering type 2 diabetes, females are especially at risk to develop uric acid stones exhibiting a subtype IIIb (37 vs. 13 % in the absence of diabetes, p < 0.00001).
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High production and excretion of uric acid from diet origin (high fructose intake, nucleo-protein rich food, rare genetic diseases on the nucleotide pathways such as Lesh–Nyhan syndrome or phosphoribosylpyrophosphate synthetase hyperactivity).
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High uric acid concentration in acidic and concentrated urine secondary to low diuresis, whatever the origin.
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Local production of ammonium ions from urea in patients with UTI by urea-splitting bacteria;
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Excessive alkaline urine secondary to alkalinization for dissolving radiolucent stones (uric acid stone suspected) in patients with a preexisting hyperuricosuria.