RENAL FAILURE DR ABD ELGHANY HEFNAWY Physiological roles

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 1. 25 (DHCC) T 4 T 3

Nephron

Blood Glucose -Bicarbonate -Na Glomerular filteration Ca, Ph, & Mg 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 PO 4 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 H 2 O reabsorption, increased plasma volume, and increased BP (aldosterone also stimulates potassium secretion into tubules)

Rennin-Angiotensin-Aldosterone System Fall in Na. Cl, extracellular fluid volume, arterial blood pressure Juxtaglomerular Apparatus Angiotension III Angioten sinase A Renin Lungs Liver + Angiotensinogen Angiotensin I Helps Correct Adrenal Cortex Converting Enzyme 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-D 3 to 1, 25 OH-D 3) 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 D 3

ﺧﻼﺻــــﺔ Functions of the Nephron Reabsorption Filtration Secretion Excretion Secretion =transferring solutes from the blood into the tubule lumen. Most important secretory products are K+, NH 4+, 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), Ca. R (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 ( Na. Cl 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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