METABOLIC EVALUATION

OF
RENAL STONE DISEASE

Dr. Apoorva Jain

 Kidney stones probably represent the
oldest documented human ailment.
 Annual incidence of 0.5% to 1.9% and a
lifetime incident rate of approximately
13% in men and approximately 7% in
women.
 The overall incidence ratio of stones in
men to stones in women 1.73.
 The recurrence rate after formation of an
initial stone is reported to be as high as 50%
at 5 yr and 80–90% at 10 yrs.
 The cost of kidney stone management was
estimated $2.1 billion in 2000.
 Prevalence is increasing.
 Diabetes and obesity.
 Changing dietary practices.
 migration from cooler rural to warmer urban settings.
 Relative lack of evidence-based guidelines for
metabolic evaluation.
 After stone passage, every patient should
undergo basic evaluation and be assigned to a
group with low or high risk of stone recurrence,
 Only high-risk stone formers require specific
metabolic evaluation individualized according
to stone type.
 Specific metabolic evaluation requires collection
of two consecutive 24-h urine samples.
 For selected pt. group like children, spot
samples may be considered (with limitations).
 Metabolic w/u to be done in stone free sate with
at least 20 days from last stone
expulsion/removal.
 After 8-12 week repeat metabolic w/u for
assessing effect of drugs-life style management.
 All stone formers, independent of their individual
risk, should follow the preventive measures,
 The main focus of these measures is
normalization of dietary habits and lifestyle risks.
BASIC EVALUATION
 Past medical history
 GI diseases - IBD/chr. diarrhea, jejuno ileal byepass – low urine vol, acidic pH
– uric acid stones. hypocitraturia and hyperoxaluria – ca-ox stones.
 Bariatric sx – ca-ox stones.
 Sarcoidosis – hypercalciuria.
 HTN/DM – metabolic syndrome/insulin resistance – uric acid stones.
 CKD – generally reduced risk (low conc. urine) but increased with MSK,
ADPKD, sjogren amd RTA.
 Drugs
 Antiretrovirals, antieplileptics, triamterene etc.
 Family history
 Genetic testing employed in sp. Cases like PH and dent’s disease (AR) and PKD
(AD).
 Socio – occupational
 Infrequent hydration and restricted toilet facility.
 Diet
 High sodium – hypercalciuria
 Animal protein – low urine pH – uric acid stones.
 Grapefruit juice/high sucrose/low dietary calcium/high dietary
oxalate(nuts/spinach/chocolate)
LAB EVALUATION
 Urinalysis,
 specific gravity and osmolality
 low urinary pH (<5.5) raises is suspect for uric acid stones. A
moderately high pH (6.5 to 7.2) may reflect complete or incomplete
distal RTA. An extremely high pH (>7.4) is usually indicative of the
splitting of urea into ammonium and bicarbonate (urease producing
organism)
 Plasma calcium, phosphorus, and uric acid.
 Parathyroid hormone (PTH), 25-hydroxycholecalciferol, and 1,25-
dihydroxycholecalciferol [1,25(OH)2D3]
 Measurements of Ca, P, oxalate, uric acid, sodium,
potassium, pH, bicarbonate, sulfate, ammonium,
titratable acid, citrate, and creatinine, and the relative
supersaturation ratios of calcium oxalate, calcium
phosphate, monosodium urate, and concentration of
undissociated uric acid should be calculated.
 Computer-based programs have the advantage of accounting
for all parameters involved and generating one number that
indicates the relative supersaturation - Equil2 , Joint Expert
Speciation System ( JESS) program.
CRYSTAL EXAMINATION
 Calcium oxalate crystals - uniform small double pyramids
that often appear as crosses in a square.

 Calcium phosphate crystals - narrow rectangular needles,

often clumped in a flower-like configuration.

 Uric acid crystals - form only in an acidic urine, which

favors the conversion of relatively insoluble urate salts
into insoluble uric acid.

 Calcium magnesium ammonium pyrophosphate (so-

called triple phosphate) crystals - form domed rectangles
that take on the appearance of coffin lids.
STONE ANALYSIS

 All attempts should be made to capture the stone and

submit it for analysis.

 Composition of stones should always be determined by x-

ray crystallography or infrared spectroscopy. Both
tests are relatively inexpensive and can lead to important
diagnoses, especially cystinuria or crystallization of drugs.

 Cystine stones are diagnostic for congenital cystinuria; a

struvite or carbonate stone is indicative of urinary tract
infection with urease-positive organisms; triamterene and
indinavir stones are pathognomonic for the precipitation of
these drugs.
 For patients with hypercalciuria and calcium
stones, measurement of BMD may be useful
 Measures for detection of genetic nephrolithiasis
- cystinuria, primary hyperoxaluria, Dent
disease, claudin mutations, and adenine
phosphoribosyltransferase deficiency.
 For patients in whom kidney stones are
suspected of having monogenic causes, more
complicated tests are performed, usually in an
academic setting; these tests include genotyping
and specific metabolic tests such as ammonium
chloride loading and urine-blood carbon dioxide
tension during bicarbonaturia (in RTA),
aminoaciduria (in Dent’s disease), and
parathyroid suppression by calcium infusion
(resulting from an activating mutation of CaSR).
RADIOLOGICAL EVALUATION
 X- Ray- accuracy of interpretation of plain radiographs is
less than satisfactory.

 Ultrasonography is less useful because visualization in the

kidney is often suboptimal, and it is almost useless for
discerning ureteral stones, although it is excellent in
detecting obstruction caused by kidney stones, safe in
children, pregnant women.

 Intravenous pyelography (IVP) has served well and been

the standard procedure for decades;

 Unenhanced computer tomography (CT) is currently the

diagnostic procedure of choice.
Metabolic evaluation and guidelines for Ca-Ox stones
Summary of treatment modality in ca-ox
stones in relation to urine abnormalities.
 pH>6.8, pH 6.5 – 6.8
infection high Ca x P

Metabolic evaluation and guidelines for Ca-po4

stones
CALCIUM STONES
 HPT nature conf. by nuclear scan
 Adenoma – Sx,
 Granuloma – ketoconazole, steroids, HCQS
 Hyperoxaluria
CALCIUM STONES Therapeutic success can be
monitored
by venous blood gas analysis
(base excess #2.0) in
complete RTA.
If excessive calcium
excretion (>8 mmol/d)
persists after
re-establishing acid-base
equilibrium, thiazides may
lower
urinary calcium excretion

Renal tubular acidosis

URIC ACID AND AMMO-URATE STONES

 Uric acid
 Dietary excess, MPD, enzyme defects, drugs,
gouts.
 Ammo-urate
 UTI, malabsorptive states(diarrhea, ileostomy,
diversions, laxative abuse).
 High urine pH >6.8
 Usually in UB, recurrent.
MANAGEMENT OF STRUVITE STONE
EVIDENCE BASED RECOMMENDATION
 Two RCTs, one on high water intake and stone
recurrence after the first idiopathic calcium
stone episode, and one on high water intake
and stone recurrence after extracorporeal
shockwave lithotripsy (ESWL), as well as large
epidemiologic studies, have indicated an
inverse relationship between high fluid intake
and stone formation.
 Level 1b/a evidence indicating that the
combination of extensive metabolic evaluation
and a tailored diet results in fewer stone
recurrences compared to limited metabolic
evaluation and general diet recommendations.
 Large epidemiologic studies have documented an
increase in the risk of kidney stones for
overweight and obese individuals. However, it is
not clear whether weight loss will lead to a
reduction in risk.
 In first-time calcium oxalate stone formers who
were followed up for 5 yr, increased fluid intake
to keep urine volume >2 l/d resulted in a 15%
absolute recurrence reduction compared to usual
fluid intake.
 In recurrent calcium stone formers who were
followed for 5 yr, adequate calcium intake (1200
mg/d), along with sodium (50 mmol/d) and
protein (52 g/d) restriction, resulted in an 18%
absolute recurrence reduction compared to
restricted calcium intake (400 mg/d).
 Trials with at least 3 yr of follow-up showed
a higher benefit for thiazide therapy.
 Two RCTs have shown that for
hyperuricosuric calcium oxalate stone
formers uric acid reduction by allopurinol is
beneficial in reducing recurrence only in the
absence of co-existing metabolic
abnormalities.
THANKS