The document discusses diseases of the urinary system. It covers the physiology of the kidneys and renal tubules, including their roles in excretion and homeostasis. Common causes of renal insufficiency and failure are described, such as decreased glomerular filtration rate. Clinical findings of urinary tract diseases include abnormal urine constituents like proteinuria, hematuria, and hemoglobinuria. The causes and pathophysiology of these urine abnormalities are explained in detail.

1. Diseases of urinary
system
Karima Al Salihi

2. Diseases of urinary system
Diseases of the bladder and urethra
are common and more important
than diseases of the kidneys in farm
animals.

3. Physiology
(1) The kidneys
They excrete the end products of tissue metabolism
(except carbon dioxide) and maintain homeostasis of
fluid and electrolyte metabolism, including acid-base
balance, by selective excretion of these substances.
The kidney maintains homeostasis by varying the
volume of water and the concentration of solutes in the
urine. The kidney composed of many similar nephrons.
Each nephron is composed of blood vessels,
glomerulus and a tubular system (proximal tubule, loop
of Henle, distal tubule and collecting duct). In general,
the tubules maintain homeostasis while the glomeruli
control excretion of metabolic end products.

6. (2) The glomerulus
•
•It is a semipermeable filter that allows easy
passage of water and low molecular weight
solutes. Glomerular filtrate is derived from
plasma by simple passive filtration driven
by arterial blood pressure. The volume of
filtrate depends on the hydrostatic pressure
and the plasma osmotic pressure in the
glomerular capillaries and on the proportion
of glomeruli which are functional.

8. (3) Renal tubules
•It reabsorbs substances (Glucose and
phosphate as the body need) which secreted
from the glomerular filtration, which are needed
for utilization and participation in metabolic
processes, while permitting the excretion of
waste products. Inorganic sulphates and
creatinine are not reabsorbed in appreciable
amounts. The tubules also actively secrete
substances, particularly electrolytes to regulate
acid-base balance and make a balance
between resorption and secretion.

9. (4) Mechanism of water regulation:
•It depends on the antidiuretic
hormone (ADH). Tissue dehydration
and an increase in the osmotic
pressure of the tissue fluid stimulate
secretion of ADH from the posterior
pituitary gland. The renal tubules
respond to ADH by conserving water
and producing concentrated urine.

10. Renal in sufficiency and renal
failure
•
•Renal insufficiency means a partial
loss of renal function. Renal failure
means that the kidneys can no
longer regulate body fluid and
solute composition. It is the
terminal stage of renal insufficiency.
•

11. • Causes of renal insufficiency, renal failure and uremia
(1) Prerenal
1) CHF and acute circulatory
failure with acute renal
ischemia
2) Hemoglobinuric and
myoglobinuric nephrosis.
3) Severe bloat can interfere
with cardiac output and lead
to renal ischemia in
ruminants.
(2) Renal
1) Glomerulonephritis, interstitial
nephritis, pyelonephritis, embolic
nephritis and amyloidosis.
2) Experimental uremia by surgical
removal of both kidneys.
(3) Postrenal:
1) Complete obstruction of the urinary
tract by vesical or urethral calculus, or
bilateral urethral obstruction.
2) Internal rupture of any part of the
urinary tract.

12. Pathogenesis
•(1) Damage to the glomerular epithelium destroys its
selective permeability and permits the passage of plasma
protein principally albumin.
•(2) Glomerular filtration may cease completely when
there is extensive damage to glomeruli.
•(3) The healthy nephrons compensate to maintain total
glomerular filtration by increasing their filtration rates
which may exceed the capacity of tubular epithelium to
reabsorb fluid and solutes causing polyuria and
developing renal insufficiency.

13. (4) Decreased glomerular filtration also results in retention
of metabolic waste products such as urea. Also phosphate
and sulphate filtration is reduced causing renal metabolic
acidosis. Phosphate retention increases calcium excretion
in the urine causing a secondary hypocalcemia.
(5) In horses, kidneys are an important rout of excretion of
calcium so the decrease glomerular rate may result in
hypercalcemia if there is a large dietary intake of calcium.
(6) Hyperkalemia can be a serious complication in renal '
insufficiency causing myocardial asthema and fatal heart
failure, which occur in uremia.
(7) Loss of tubular resorptive function causes loss of
sodium; hyponatremia which occurs in all cases of renal
failure resulting in clinical dehydration.

14. (8) The terminal stage of renal insufficiency “renal
failure” is the result of the cumulative effects of
impaired renal excretory and homeostatic functions.
Continued loss of large volume dilute urine causes
dehydration.
(9) Prolonged hypoproteinemia results in rapid loss of
body condition and muscle weakness. Acidosis is also
a contributing factor to muscle weakness and mental
attitude. Hyponatremia and hyperkalemia cause
skeletal muscle weakness and myocardial asthema.
(10) Renal failure and urinary tract obstruction cause
uremia. It is characterized by an increase in blood
urea and creatinine (azotemia) and by retention of
other solutes.

15. Clinical findings
•
(1) Abnormal constituent of the urine
(2) Variations in daily urine flow
(3) Abdominal pain and painful and
difficult urination (dysurea and
stranguria).
(4) Abnormal size of the kidneys.
(5) Abnormalities of the bladder and
urethra.
(6) Acute and chronic renal failure.

16. Principle manifestation of urinary tract
diseases
(1)Abnormal constituents of the urine
(1) Proteinuria
• Causes
(1) Normal urine contains only small amount of protein. It is
more observed in normal foals, calves, kids and lambs in
the first 40 hours after they receive colostrum.
•
(2) Transitional due to:
•
1) Physiological condition.
2) Excessive muscular exercise.
3) Emotional stress and convulsion.
4) Excessive ingestion of protein.

17. (2) Pathological: It may be:
1) Pre renal: e.g. congestive heart
failure, myoglobinuria, hematuria and
hemoglobinuria. Small amounts are
associated with fever and toxemia.
2) Renal: e.g. Glomerulonephritis, renal
infarction, tubular nephrosis, amyloidosis
and urinary tract infections.
3) Post renal: e.g. urinogenitial tract
infections (cystitis, prostitis, uretheritis,
ureteritis).

18. Pathogenesis
(1) Plasma protein enters urine when glomerular
permeability is increased as well as tubular cell
degeneration in cases of acute tubular nephrosis.
(2) Proteinuria can be quantified by determining
amount of protein passed in a 24-hour period or
by urinary creatinine. The highly alkaline urine
produced by herbivores can result in a false
positive reaction for protein.
(3) Chronic and acute proteinuria may cause
hypoproteinemia as occurs in chronic
glomerulonephritis and acute tubular nephrosis in
horses and in amyloidosis of cattle.

19. (2) Casts and cells
(1) Casts are organized, tubular structures, which
vary in appearance depending on their composition.
(2) It is indication of inflammatory or degenerative
changes in the kidney where they form by
agglomeration of desquamated cells and Tamm-
Horsfall protein.
(3) Casts may not form in all cases of renal
disease.
(4) Casts readily dissolve in alkaline urine and are
best detected in fresh urine samples.
(5) Erythrocytes, leukocytes and epithelial cells in
urine may originate in any part of the urinary tract.

20. (3) Hematuria
It is the presence of red blood cells or clots in the urine
(1) Prerenal causes
such as:
1) Trauma to the kidney.
2) Septicemia (Anthrax,
Leptospirosis,
Hemorrhagic septicemia)
and purpura
hemorrhagica.
(2) Renal causes
include:
1) Acute
glomerulonephritis.
2) Renal infarction
3) Embolism of the renal
artery.
4) Pyelonephritis
5) Tubular damage by
sulphonamide, arsenic,
phosphorus and lead
toxicity.
3) Postrenal causes: may
occur in:
1) Urolithiasis.
2) Cystitis.
3) Faulty catheterization.
4) Blood from the
reproductive tract.
5) Enzootic hematuria of
cattle when hemorrhage
originates from tumours
of the urinary bladder.

21. •NB: In severe cases of hematuria, blood
may be voided as grossly visible clots or
deep red to brown colored urine.
•NB: Less severe cases may show only
cloudiness which settles to form a red
deposit on standing.
•NB: In slight condition detected only on
microscopic examination of a centrifuged
sediment.
•NB: Hematuria for long periods result in
blood loss anemia.

22. (4) Hemoglobinuria
•It is a presence of hemoglobin in urine
Causes: See also post parturient hemoglobinuria.
(1) False: It occurs in hematuria when erythrocytes are
lyses and release their hemoglobin. In this case,
erythrocytes can be detected only by microscopic
examination of urine sediment for cellular debris.
(2) True: It causes a deep red to brown coloration of urine.
It gives a positive reaction to biochemical tests for
hemoglobin. There is no erythrocyte debris in sediment.

23. (3) Hemoglobin liberated from circulating erythrocytes is
converted to bile pigments in the cells of the
reticuloendothelial system. If hemolysis exceeds the
capacity of this system to remove the hemoglobin, it
accumulates in the blood until it exceeds a certain renal
threshold and then passes into the urine.
(4) Some hemoglobin is reabsorbed from the glomerular
filtrate by the tubular epithelium.
(5) Hemoglobin precipitates to form casts in the tubules,
especially if the urine is acidic and as a result some
plugging of tubules occurs, but the chief cause of uremia in
hemolytic anemia is ischemic tubular nephrosis.