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RENAL FAILURE
DR / ABD ELGHANY HEFNAWY
Physiological roles of the kidney
Maintainance of blood
and fluids electrolytes
haemostasis
Clearing of metabolites
and nitrogenous wast
products
-Urea
-Creatinine
-Uric acid
-Ammonia
-Na, K & Cl
-Ca, Ph & Mg
-Bicarbonate
Hormones & enzymes
Erythropiotine
Erythropiosis
Renine
5 type I deiodinase
α-Hydroxylase
Regulates secretion
of aldesterone
T4
1.25 (DHCC)
T3
Nephron
Blood
Glucose
-Bicarbonate
-Na
Glomerular
filteration
Ca, Ph, & Mg
Na & K
-Na & K
-Cl
Blood
Functions of the Kidneys
A. Homeostatic Functions
1. Waste excretion (urine formation)
a. Nitrogenous end products: urea, creatinine, uric acid,
etc.
b. Metabolic degradation of peptide hormones: glucagon,
insulin, PTH, growth hormone, FSH, and gastrin.
2. Fluid/electrolyte balance (Na+, K+, water)
3. Acid/base regulation:
• kidneys generate and reclaim filtered bicarbonate, as well
as secrete excess acid to maintain balance.
4. Balance of other electrolytes (Ca++, Mg++,
Phosphate PO4 3-)
B. Non-excretory functions
1. Renin-angiotensin mechanism to control BP(Blood
Pressure
a. Kidney senses decreased BP
b. Secretes renin (enzyme), which converts Angiotensin I
to angiotensin II
c. Angiotensin II is a vasoconstrictor  increased BP
d. Angiotensin II also stimulates aldosterone secretion
e. Aldosterone increases Na+ and H2O reabsorption,
increased plasma volume, and increased BP
(aldosterone also stimulates potassium secretion into
tubules)
Rennin-Angiotensin-Aldosterone System
Fall in NaCl, extracellular fluid volume, arterial blood pressure
Juxtaglomerular
Apparatus
Angiotension III
Angioten
sinase A
Renin
Lungs
Liver
+
Angiotensinogen
Helps
Correct
Adrenal
Cortex
Converting
Enzyme
Angiotensin I
Angiotensin II
Aldosterone
Increased
Sodium
Reabsorption
2. Produces erythropoietin
a. Stimulates erythropoiesis in bone marrow
b. The anemia of CRF is primarily caused by
impaired erythropoiesis
c.  RBC formation is mainly due to  erythropoietin
production in the diseased kidneys, although
other compounds that accumulate in renal
failure may also suppress erythropoiesis.
3. Maintains Calcium-Phosphorus bone
homeostasis
a.
Activates Vitamin D (Hydroxylation of 25-OH-D3 to
1,25-OH-D3) in kidney disease, can supplement
calcitriol, but very expensive Low vit. D  less Ca++
absorbed
b. Inverse relationship between Ca++ and P, so when P is
retained by diseased kidney, Ca++ levels decline (less
calcium reabsorbed by the kidney).
c. Low serum calcium  parathyroid gland releases PTH:
Parathyroid Hormone: works to elevate serum Ca++
by pulling it from the bones  fragility, muscular
weakness, decreased muscular tone, and general
neuromuscular hypoexcitability.
Vitamin D from UV exposure
Active Vit D3
‫خالصــــة‬
Functions of the Nephron
Reabsorption
Filtration
Secretion
Excretion
Secretion =transferring solutes from the blood into the tubule lumen.
Most important secretory products are K+, NH4+, and H+.
Definition
Sudden inability of kidney for clearing of the
metabolites, nitrogenous wast products or
maintanance of blood and fluids electrolytes
haemostasis.
Anaemia
High levels of urea
and creatinine
Azotemia
Etiology
Post-renal
Azotemia
Pre-renal
-Dehydration
-Hyperthermia
-Heart and circulatory
diseases
-Renal ischemia
-Hypovalemic chock
-Haemolytic anemia
_Haemorrhage
Renal
-Nephritis
-Glomerulonephritis
-Pyelonephritis -Nephrosis
-Nephrotoxin
(Aminoglycosides,Hb,
Myoglobine & heavy metals)
Trauma - Cancer-Coryn.,Leptospirosis
& Streptococus
-Obstruction of
collecting system
-Urolithiasis
-Uretheral obstructoin
-Rupture of UB
-Obstruction of ureters
-Paralytic bladder
Damage of kidney
Pathogenesis
Etiology and predisposing
factors
Damage of the functional and
structural unite of the kidney ( nephron)
Pathological and biochemical alterations
Inability of the kidney for performing
their physiological roles
Clinical signs of kidney damage or RF
Myoglobinuria
Myoglobin
Nephrotoxine
Renal Failure
Renal azotemia
Anorexia
Triglyceride
Gluconeogenesis
Hyperlipemia
Damage
of nephron
Clinical signs
( Non-specific)
1- Intermittente fever
( if infectious causes are suspected).
2-Polyuria in case of renal azotemia.
3-Oliguria in case pre-renal azotemia.
4-Anuria or dysuria in case of
pos-trenal azotemia.
5- Anorexia and weakness.
6-Decreased performance.
7-Odema due to proteinuria.
8-Abdominal palpation show painful
enlarged kidney.
9- Specific signs according to
the etiolgical factors.
Abdominal pain
Thirst
Stomatitis with tongue ulcer
Dehydration
Gastrointestinal disturbances in
CRF
Oral lesions
• Foul odor
• Stomatitis
• Erosions and
ulcers
• Tongue tip
necrosis
(fibrinoid
necrosis and
focal ischemia)
VD (Vitamin-D), VDR (Vitamin-D Receptors), CaR (Calcium Receptors)
Laboratory finidings
Blood
-Acidosis
-Anaemia
-Haemoconcentration
-Increased PCV
Serum
-Hyponatremia (Na)
-Hypokalemia (K)
-Hypochloremia (Cl)
-Hypocalcemia ( Ca)
-Hypoproteinemia
-Hypoglycemia
-Hyperlipemia
-Increased urea and
creatinine levels
-Hypophosphatemia
Urine
-Low specific
gravity
-Hematuria
-Pyoueria
-Haemoglobinuria
-Presence of
crystals
Diagnosis
1- History and clinical signs
2- Laboratory findings
3- X-rays
4- Ultrasonography
Treatment
-Correction of electrolytes and fluid balance.
-Identification and treatment
of underlying diseases.
-Supportive treatment.
-Treatment of complications
-Fluid therapy
-Dextrose 5% ( IV)
-Sodium Bicarbonate 5% (IV)
-Oral fluids by nasogastric tube
-Saline ( NaCl 0.9%) IV
-Antimicrobial drugs.
-Diuretic for flushing
the kidney ( furosemide
as Lasix).
-Flunixine meglumine
(0.25 mg/ kg).
Treatment of secodnary complcations
As:-Stomatitis
-Urine scalding
-Hyperlipemia
Thanks alot for your patience
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