Page 130 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Urolithiasis
Concrement-forming substances (→ A1) can Abnormal renal reabsorption is a frequent
reach concentrations in the urine that lie cause of increased renal excretion in hypercal-
above their solubility threshold. In the so- ciuria and an invariable cause in cystinuria
called metastable range the formation of crys- (→ p. 96). The Ca 2+ concentration in blood is
tals may not occur at all, or only slowly, despite then maintained by the intestinal absorption
supersaturation of the solution. However, and mobilization of bone minerals, while the
when the concentrations rise beyond the cystine concentration is maintained by a re-
metastable range, crystallization occurs. Dis- duced breakdown.
Kidney, Salt and Water Balance kidney stones are calcium oxalate (ca. 70%), urine concentration (→ A4).
solving already formed crystals is possible
Release of ADH (in volume depletion, stress,
only by reducing the concentration to below
etc.; → p. 260) leads to a raised concentration
of stone-forming substances via enhanced
the metastable range.
The most frequently found components in
The solubility of some substances depends
calcium phosphate or magnesium-ammonium
on the pH of urine. Phosphates are easily dis-
solved in an acidic urine, but poorly in an alka-
phosphate (ca. 30%), uric acid or urate (ca.
30%) as well as xanthine or cystine (< 5%). Sev-
line one. Phosphate stones are therefore, as a
rule, only found in alkaline urine. Conversely,
eral substances may be contained in one stone,
ated than undissociated, and uric acid stones
as nuclei for crystallization and facilitate the
deposition of other metastably dissolved sub-
are formed more readily in acidic urine. If the
formation of NH 3 is reduced, the urine has to
stances (hence the total is > 100%).
5 because crystals that have already formed act uric acid (urate) is more soluble when dissoci-
Certain substances that form complexes, be more acidic for acid to be eliminated, and
such as citrate, pyrophosphate, and (acid) this promotes the formation of urate stones.
phosphate, can bind Ca 2+ and, by reducing the A significant factor is also how long crystals
Ca 2+ concentration, are able to prevent calcium that have already formed actually remain in
phosphate and calcium oxalate from precipi- the supersaturated urine. The length of time
tating. depends on the diuresis and the flow condi-
Causes of stone formation. The raised con- tions in the lower urinary tract that can, for ex-
centration of stone-forming substances can be ample, lead to crystals getting caught (postre-
the result of prerenal, renal, and postrenal fac- nal cause).
tors: The effect of urolithiasis is that it blocks the
Prerenal causes produce the increased filtra- lower urinary tract (→ A5). In addition,
tion and excretion of stone-producing sub- stretching of the ureteric muscles elicits very
stances via a raised plasma concentration painful contractions (renal colic). Obstruction
(→ p. 94). Thus, prerenal hypercalciuria and to flow leads to ureteral dilation and hydrone-
phosphaturia are the result of raised intestinal phrosis with cessation of excretion. Even after
absorption or mobilization from bone, for ex- removal of a stone, damage to the kidney may
ample, if there is an excess of PTH or calcitriol persist. The urinary obstruction also promotes
(→ A2). Hyperoxalemia can be brought about growth of pathogens (urinary tract infection;
by a metabolic defect in amino acid break- pyelonephritis; → p.106). Urea-splitting patho-
down or by increased intestinal absorption gens form NH 3 from urea, thus alkalinizing the
(→ A3). Hyperuricemia occurs as a result of urine. This in turn, in a vicious circle, favors the
an excessive supply, increased new synthesis, formation of phosphate stones. Even without
or increased breakdown of purines (→ A3). bacterial colonization, intrarenal deposition of
Xanthine stones may occur when the forma- uric acid (gouty kidney) or of calcium salts
tion of purines is greatly increased and the (nephrocalcinosis) can result in inflammation
breakdown of xanthines to uric acid is inhib- and destruction of renal tissue.
ited. However, xanthine is much more soluble
120 than uric acid and xanthine stones are there-
fore much less common.
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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