D’YOUVILLE COLLEGE
BIOLOGY 307/607 - PATHOPHYSIOLOGY
Lecture 16 - URINARY DISORDERS
Chapter 15
1.
Anatomy & Physiology of Kidney (& Urinary Tract):
• kidney (fig. 15 - 1 & ppt. 1):
- outer cortex, inner medulla (divided into pyramids)
- urinary tract: pyramids release newly formed urine into calyces that
merge into renal pelvis (inside hilum -- medial, concave margin of kidney; ureters
extend away from pelvis & descend posterior abdominal wall to urinary bladder
- urinary bladder: temporarily stores urine & excretes it via urethra
• functions of kidney:
- excretion: nitrogenous wastes (urea, uric acid, & creatinine); any materials
present in excessive amounts (hydrogen ion, sodium, potassium, etc.)
- regulation: regulates blood formation via erythropoietin
- regulates blood pressure via renin-angiotensin system
• nephron (fig. 15 - 2 & ppt. 2): renal tubule that receives circulation from two
sets of arterioles (afferent & efferent) that supply two sets of capillaries (glomeruli &
peritubular capillaries, respectively) (fig. 15 - 4 & ppt. 3)
- renal tubule consists of Bowman's capsule that receives filtrate from
glomerulus (first capillary, supplied by afferent arteriole); glomerulus has extremely
leaky membrane (figs. 15 - 3, 15 - 6 & ppts. 4 & 5)
- proximal convoluted tubule: receives filtrate from Bowman's capsule &
processes it by absorbing many substances back into blood in peritubular capillaries;
accomplishes majority of reabsorption without hormonal regulation (obligatory)
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- loop of Henle: tubular loop with hairpin bend; important in establishing
nephron's capability of varying water reabsorption
- distal convoluted tubule: also processes tubal fluid (like proximal tubule) but
depends on hormones to vary reabsorption activity (facultative)
- collecting duct: receives tubal fluid from numerous nephrons, completes
processing of fluid to urine, excretes urine from medulla
• physiology (fig. 15 - 5 & ppt. 6):
- filtration: glomerulus has extremely leaky membrane (fig. 15 - 3 & ppt. 5)
& conducts only filtration of blood -- approximately 20% of plasma volume filters out
of blood to Bowman's capsule -- 125 ml./min. = 180 liters/day (= glomerular filtration
rate)
- reabsorption: recovers approx. 124 ml./min. resulting in 1 ml./min. urine
output = 1.5 liters/day
- secretion: substances added to urine by tubule cells
- urine formation: substances filtered from plasma & not reabsorbed + substances
secreted by tubule cells
2.
Renal Disease: usually manifests as waste retention &/or fluid, electrolyte
or acid/base imbalance
• glomerulonephritis (GN): any disruption of glomerular filtration produces
disorders involving failure to excrete toxic wastes or failure to recover needed
substances
- pathogenesis: (fig. 15 - 8 & ppt. 7) results from immune attack (immune
complexes in 70 % of cases) on glomerular membranes with resultant infiltration by
phagocytes, complement activation, platelet activation, & formation of microthrombi
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(fig. 15 - 9 & ppt. 8); may be cellular proliferation & thickening of basement
membrane
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- antigens may derive from streptococcal infections, or hepatitis viruses that
promote immune complex formation (fig. 15 - 9 & ppt. 8); less frequently, autoantibodies
are involved (fig. 15 - 10 & ppt. 9)
- sequelae of GN: nephrotic syndrome involves pattern of glomerular
damage that produces protein loss in urine (fig. 15 - 11 & ppt. 10)
- increased protein in urine (proteinuria), decline in plasma protein
levels, especially albumins (hypoalbuminemia), widespread edema (due to loss of
plasma protein osmotic pressure), & elevated blood lipids (hyperlipidemia)
- other specific protein losses account for increased susceptibility to infection
(loss of immunoglobulins), or thrombosis (loss of anticoagulants)
- nephritic syndrome involves pattern of glomerular damage that produces
blood loss in urine with lower level of protein loss, accompanied by reduced
glomerular filtration (fig. 15 - 12 & ppt. 11)
- blood loss in urine (hematuria), less proteinuria, retention of water
resulting in reduced urine output (oliguria), & retention of nitrogenous wastes
(azotemia)
• pyelonephritis: infective condition that may derive from blood-borne bacteria
(descending or hematogenous); usually targets medulla, calyces & renal pelvis
- much more frequently, invasion of lower urinary tract infections (ascending)
is the etiology (fig. 15 - 13 & ppt. 12)
- acute attacks may be resolved after short period of illness, with antibiotic
treatment; pus in urine may be found (pyuria)
- chronic conditions are usually more dangerous; because of kidneys' large
nephron reserve, extensive necrosis may have occurred before detectible signs are evident
and renal failure, necessitating dialysis or transplant, is often the result
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• interstitial nephritis: toxic attack on kidney interstitial compartment;
endogenous (bacterial toxins) or exogenous toxins (drugs, antibiotics, or toxic
chemicals) may be involved (table 15 - 2)
• renal vascular diseases: various conditions that may cause renal ischemia, e.g.
hypotension, atherosclerosis with embolisms, diabetic GN or arteriolosclerosis
(nephrosclerosis); nephrosclerosis may be benign (low risk) or malignant (high risk of
renal failure)
• urolithiasis: formation of stones in the urine, usually in the kidney, but also in
lower urinary tract; most are formed from calcium (calculi), due to hypercalcuria; most
may be passed uneventfully but renal colic (excruciating pain) may occur with a large
stone that obstructs a vessel
• classification of renal disorders (fig. 15 - 16 & ppt. 13): renal (intrarenal)
disease involves causes originating within kidney; prerenal disease involves causes
of renal ischemia (fig. 15 - 17 & ppt. 14); postrenal disease involves obstructions of
urinary tract
3.
Renal Failure:
• uremia: consequence of accumulation of wastes in blood, fluid imbalance, &
electrolyte imbalance; while virtually the entire body suffers from uremia,
encephalopathies & pericarditis are particularly serious sequelae; symptomatic of end stage
failure & usually lethal
• acute renal failure: rapidly progressing renal dysfunction, usually caused by
tubular necrosis due to toxins or to ischemia; usually resolved by regeneration of tubules
• chronic renal failure: more severe, gradual deterioration of kidney parenchyma
that usually follows chronic glomerulonephritis or chronic pyelonephritis; usually proceeds
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to development of uremia; treat with dialysis and/or kidney transplant ( figs. 15 -19
to 15 - 21 & ppts. 15 to 17)