Page 116 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Interstitial Nephritis
The term interstitial nephritis is applied to in- Massive administration of prostaglandin-
flammatory changes in the kidney if the in- synthesis inhibitors can damage the renal me-
flammation does not originate in the glomeru- dulla by causing ischemia. In normal circum-
li. Renal tissue is infiltrated by inflammatory stances renal medullary perfusion at low per-
cells (especially granulocytes) and the inflam- fusion pressure is maintained by the release
mation can lead to local destruction of renal of vasodilating prostaglandins. Inhibition of
tissue. prostaglandin synthesis stops this protective
The most common form of interstitial ne- mechanism, however.
Kidney, Salt and Water Balance cending pyelonephritis]); less often in the blood lies within the renal medulla (loop of Henle
phritis is that caused by bacteria (pyelonephri-
In accordance with the site of the inflamma-
tis). Most often the infection originates in the
tory processes, the first effects are caused by
lesions in the segment of the nephron that
urinary tract (bladder → ureter → kidney [as-
(descending pyelonephritis) (→ A1). The renal
and collecting duct). A relatively early occur-
rence is reduced urinary concentration, caused
medulla is practically always affected first, be-
by damage to the ascending part, by flushing
cause its high acidity, tonicity, and ammonia
concentration weaken the body’s defense
out of the medulla as a result of inflammatory
mechanisms. Flushing out the renal medulla
hyperemia as well as by a lack of sensitivity of
creased urine volume causes nocturnal di-
is promoted by an obstruction to urinary flow
+
(urinary tract stone [→ p.120], pregnancy [→
uresis (nycturia). The decreased K secretion
into the collecting duct can cause hyperkale-
p.116], prostatic hypertrophy, tumor) and by
5 thus lowers the danger of infection. Infection the damaged distal nephron to ADH. The in-
+
reduced immune defenses (e.g., diabetes mel- mia, while reduced Na reabsorption can re-
litus [→ p. 290]). sult in hypovolemia (→ A3). However, the re-
+
An interstitial nephritis can also cause the duced Na reabsorption in the loop of Henle
+
deposition of concrements (calcium salts, uric can also result in an increased distal K secre-
acid) in the renal medulla without any infec- tion with accompanying hypokalemia, espe-
tion (→ A2). Uric acid deposits in the kidney cially when more aldosterone is released as
are principally caused by an excessive dietary the result of hypovolemia (→ p. 266).
intake of purines, which are broken down in Renal acid excretion can be impaired, re-
the body into uric acid, as well as by a massive sulting in an alkaline urine being formed and
increase of endogenous uric acid production, also in systemic acidosis.
as occurs in the leukemias and in rare cases of Various functions of the proximal tubules
enzyme defects of uric acid metabolism (reabsorption of glucose and amino acids, se-
(→ p. 250). Calcium deposits are the conse- cretion of PAH) and the glomeruli (GFR) are af-
quence of hypercalciuria that occurs when in- fected only in advanced pyelonephritis.
testinal absorption of calcium is increased Infection by urea-splitting pathogens leads
(e.g., in hypervitaminosis D) as well as with in- to a breakdown of urea into ammonia in the
creased mobilization of calcium from bone urine. As ammonia binds hydrogen ions
(e.g., by tumors, immobilization; → p.132). (→ A4), an alkaline urine will result. This pro-
Lastly, interstitial nephritis can result from motes the precipitation of phosphate-contain-
toxic (e.g., phenacetin) or allergic (e.g., penicil- ing concrements (→ p.120) that in turn can
lin) factors, from radiation or as a rejection re- cause obstruction to urinary flow and thus the
action in a transplanted kidney. The renal me- development of ascending pyelonephritis, i.e.,
a vicious circle is established.
dulla is especially prone to hypoxia because O 2
diffuses from the descending to the ascending
limb of the vasa recta. In sickle cell anemia
(→ p. 36) deoxygenation therefore leads to
precipitation of hemoglobin, especially in the
106 renal medulla, and thus to vascular occlusion.
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
All rights reserved. Usage subject to terms and conditions of license.