lec 51 .... Dr. Su3ad-7-
RENAL FAILURE :
It’s the failure of the kidney to perform normal function which is the excretion of body metabolite and control of fluid and electrolyte and PH of the blood and hormonal function , so the result of this failure is the retention of urea and creatinine (u&c) and fluid and electrolyte disturbance ( increase k, and decrease in Ca ) and endocrine change as erythropoietine which lead to anemia .
We divide RENAL FAILURE to ACUTE and CHRONIC .
ACUTE RENAL FAILURE (ARF): this is renal failure developed over a short period of time over hours , days and sometimes weeks , and become symptomatic most of ARF is reversible but not all the cases we should diagnose it by decrease urine output (uop) or anuria or oliguria ,,,, but sometimes we may have increase uop ,,, we also have increase u&c and k+
CAUSES OF ARF:
We divide it into three categories ,,,,
1.renal 2.prerenal 3.postrenal
Now we will discus all the above in details .
1. PRERENAL : this mean decrease or interfere with the blood supply to the kidney so the causes is the following ….
1. hypovolemia : - decrease in cardiac out put
- loss of blood as in bleeding
- loss of fluid and is DM or DI
- in renal tubular damage this lead to salt deplesion which lead to decrease in blood volume .
-hypoprotienemia
-third space fluid loss this occur in serious ill patient as in stomach distention and fluid accumulation in it .
2. heart failure : this will lead to decrease cardiac output and decrease GFR this also may be due to myocardial infarction or valvular function or cardiac temponade .
3. systemic vasodilatation :this due to pooling of blood in the vessels this will lead to decrease in the blood volume and lead to decrease in the kidney perfusion ,,,,, causes sepsis , cirrhosis ,anaphylaxis ,anesthesia , pharmacological vasodilatation .
4. impair renal autoregulation :
Preglomerular vasoconstriction :
-sepsis, hypercalcemia ,hepatorenal syndrome
-drugs :NSAIDS, cyclosporine ,amphotrecine B, epinephrine ,nor epinephrine .
5. postglomerular vasodilatation : this will lead to decrease in the pressure in the glomerular blood vessels tuft which lead to decrease filtration of substances .
- ACEI
- angiotensin AT1 recptor antagonist .
NOW FOR …..
RENAL CAUSES OF THE ARF:
1. intrarenal vascular insult : here the disease is mainly systematic ( the disease of the vascular system ) as ,,,,
vasculitis ,haemolytic uremic syndrome , thrombotic thrombocytopenic purpura ,accelerated hypertension .
2. GN any kind of GN if sever enough may lead to ARF .
3. ischemic acute tubular necrosis
4. toxic acute tubular necrosis :here the tubules is affected is due to the accumulation of these substances in the tubules so it’s the major affected sites .
-endogenous toxins :myoglobulinemia ,haemolytic uremic syndrome , urate crystals , high level of bilirubin ,hypercalcemia .
-exogenous toxins : -drugs :amphotrecine B ,aminoglycosides ,vancomycine ,cisplatin ,acetaminophene
-contrast nephrotoxicity .
- drugs crystalluria , as acyclovir , methotrexiate ,sulphoneamide ,trimethoprime .
5. renal arterial or vein occlusion .
6. renal interstitial nephritis (IN):
-acute allergic IN : antibiotics ,sulphoneamide ,NSAIDS ,capotine .
-bilateral acute pylonephritis
-malignant infiltration of kidneys ,, lymphoma , leukemia , sarcoidosis .
7. intertubular obstruction :
-casts as in myloma .
-crystals .
Now for POSTRENAL causes : this should be bilateral lower urinary tract obstruction as in bladder neck or urethral obstruction :
-stone ,infiltration, tumors .
- fibrosis , adhesion .
In this postrenal we usually have anuria so when we have anuric ARF we should this of postrenal causes .
CLINICAL MANIFESTATION :
• follow the insult by hours ,days , weeks .
• usually we have decrease the urine output or may have anuria but sometimes we may have increase urine output this happen in the tubular damage (necrosis).
• Fluid retention ,increase body weight , edema ,hypertension , decrease GFR ,increase U&C especially in catabolic state as sepsis .
• Increase serum k+ occur
• Metabolic acidosis H+ retention
Note : increase the k+ and metabolic acidosis is the factors that kills the patient .
• Decrease in Ca, increase in p , uric acid , anemia this will develop after few days .
• Uremic symptoms : appear later in the disease and gradually and depend on the cause : as anorexia ,nausea ,vomiting ,irritability ,muscle twitching ,increase reflexes ,convulsion , coma ,GI bleeding ,increase suseptability to infection cos decrease in immunity .
RECOVERY PHASE :
Most of the patients get better by stopping the causative insult and by giving medications to the patient but this recovery happen slowly as increase urine output and GFR and decrease in U&C .
IVx:
• Anuria suggest lower urinary tract obstruction , may complicate sever prerenal , serious GN ,vessels obstruction
• In partial urinary tract obstruction can present as polyuric .
• Prerenal uremia : urine analysis is not helpful cos there is very low renal output .
• Pigmentation (muddy brown ) characteristics of tubular necrosis , suggest ischemia or nephrotoxic .
• Red cell cast indicate glomerular insult
• White cell count interstitial nephritis .
• Broad granular cast indicate chronic renal disease
• Eosinophilic cells , in antibiotic induced allergic nephritis .
• Lymphocytes ,, indicate NSAID use .
Dx : history in
1. volume depleted : thirst ,dry mouth ,oliguria ,decrease in JVP,BP , excessive fluid loss , dry skin , postural hypertension , tachycardia .
2. volume gain : fluid overload appear as ankle odema (pitting ) ,, third heart sound , increase JVP,BP, pulmonary edema ,effusion .
urine chart in ARF :
diagnositic index prerenal interstitial renal
frac Na exam <1 >1
urine Na con <10 >20
urine cr/plasma cr >40 >20
urine ur/plasma ur >8 <3
urine specific gravity >1.018 <1.015
urine osmolarity >500 <300
plasma bun/cr ratio >20 >1
bun =blood urea nitrogen
renal function index <1 >1
Rx:
• treat the underlying cause .
• oliguric phase restrict fluid and electrolyte intake .
• restrict intake of protein to less 20g/day or stop intake if the condition is sever and instead increase the CHO intake .
• give diuretic in oliguric phase .
specific conditions treatment :
1.increase k+ level : restrict the k+ contain food , dialysis is the main treatment of k+ increase
• urgent Ca gluconate IV
• insuline intake + dextran 50% 50 ml IV ,salbutamol 0.5%-1% IV slowly or 10-20mg calcium resonium
• NaHCO3 4.2% 100mg over 5 minutes
• Dialysis is the main treatment
2.pulmonary edema :
• Oxygen with bronchodilator
• Increase the dose of diuretic till 1gm frusemide +nitroglycan 10-20mg/min
• Morphine 5mg IV
• Dialysis is the main treatment
• Sometime do venesection and take 100 ml of blood or do torniquent this is to decrease venous return .
3. metabolic acidosis :
• NaHCO3
• Dialysis
• Monitor PH and Ca level
4. hypertensive encephalopathy : Headache , check fundi ,fits , coma .
So protect the airway , and give valium for fits and if get the needed benefit use phynitoin 300mg if in coma use sodium valeproate 10mg/kg and gradual decrease in blood pressure gradually .
5. uremic encephalopathy :
• Dialysis
• Sodium valeproate ,phynitoin
6. pericarditis :
• Frequent dialysis is the best treatment
• NSAIDS to relief pain and inflammation
7. cardiac temponade : need aspiration of the fluid then frequent dialysis .
DIALYSIS : indicated in the following occasions
1. sever acidosis
2. intractable volume overload
3. increase k+level not relived by treatment
4. prophylactic in urea >100-150mg/dl or Cr level >8-10mg/dl
5. uremic encephalopathy
done by : Y.I.ZAKKO
and medicine group :
Ali Rasheed
raghad ali
farah baha
siran mahrous
RENAL FAILURE :
It’s the failure of the kidney to perform normal function which is the excretion of body metabolite and control of fluid and electrolyte and PH of the blood and hormonal function , so the result of this failure is the retention of urea and creatinine (u&c) and fluid and electrolyte disturbance ( increase k, and decrease in Ca ) and endocrine change as erythropoietine which lead to anemia .
We divide RENAL FAILURE to ACUTE and CHRONIC .
ACUTE RENAL FAILURE (ARF): this is renal failure developed over a short period of time over hours , days and sometimes weeks , and become symptomatic most of ARF is reversible but not all the cases we should diagnose it by decrease urine output (uop) or anuria or oliguria ,,,, but sometimes we may have increase uop ,,, we also have increase u&c and k+
CAUSES OF ARF:
We divide it into three categories ,,,,
1.renal 2.prerenal 3.postrenal
Now we will discus all the above in details .
1. PRERENAL : this mean decrease or interfere with the blood supply to the kidney so the causes is the following ….
1. hypovolemia : - decrease in cardiac out put
- loss of blood as in bleeding
- loss of fluid and is DM or DI
- in renal tubular damage this lead to salt deplesion which lead to decrease in blood volume .
-hypoprotienemia
-third space fluid loss this occur in serious ill patient as in stomach distention and fluid accumulation in it .
2. heart failure : this will lead to decrease cardiac output and decrease GFR this also may be due to myocardial infarction or valvular function or cardiac temponade .
3. systemic vasodilatation :this due to pooling of blood in the vessels this will lead to decrease in the blood volume and lead to decrease in the kidney perfusion ,,,,, causes sepsis , cirrhosis ,anaphylaxis ,anesthesia , pharmacological vasodilatation .
4. impair renal autoregulation :
Preglomerular vasoconstriction :
-sepsis, hypercalcemia ,hepatorenal syndrome
-drugs :NSAIDS, cyclosporine ,amphotrecine B, epinephrine ,nor epinephrine .
5. postglomerular vasodilatation : this will lead to decrease in the pressure in the glomerular blood vessels tuft which lead to decrease filtration of substances .
- ACEI
- angiotensin AT1 recptor antagonist .
NOW FOR …..
RENAL CAUSES OF THE ARF:
1. intrarenal vascular insult : here the disease is mainly systematic ( the disease of the vascular system ) as ,,,,
vasculitis ,haemolytic uremic syndrome , thrombotic thrombocytopenic purpura ,accelerated hypertension .
2. GN any kind of GN if sever enough may lead to ARF .
3. ischemic acute tubular necrosis
4. toxic acute tubular necrosis :here the tubules is affected is due to the accumulation of these substances in the tubules so it’s the major affected sites .
-endogenous toxins :myoglobulinemia ,haemolytic uremic syndrome , urate crystals , high level of bilirubin ,hypercalcemia .
-exogenous toxins : -drugs :amphotrecine B ,aminoglycosides ,vancomycine ,cisplatin ,acetaminophene
-contrast nephrotoxicity .
- drugs crystalluria , as acyclovir , methotrexiate ,sulphoneamide ,trimethoprime .
5. renal arterial or vein occlusion .
6. renal interstitial nephritis (IN):
-acute allergic IN : antibiotics ,sulphoneamide ,NSAIDS ,capotine .
-bilateral acute pylonephritis
-malignant infiltration of kidneys ,, lymphoma , leukemia , sarcoidosis .
7. intertubular obstruction :
-casts as in myloma .
-crystals .
Now for POSTRENAL causes : this should be bilateral lower urinary tract obstruction as in bladder neck or urethral obstruction :
-stone ,infiltration, tumors .
- fibrosis , adhesion .
In this postrenal we usually have anuria so when we have anuric ARF we should this of postrenal causes .
CLINICAL MANIFESTATION :
• follow the insult by hours ,days , weeks .
• usually we have decrease the urine output or may have anuria but sometimes we may have increase urine output this happen in the tubular damage (necrosis).
• Fluid retention ,increase body weight , edema ,hypertension , decrease GFR ,increase U&C especially in catabolic state as sepsis .
• Increase serum k+ occur
• Metabolic acidosis H+ retention
Note : increase the k+ and metabolic acidosis is the factors that kills the patient .
• Decrease in Ca, increase in p , uric acid , anemia this will develop after few days .
• Uremic symptoms : appear later in the disease and gradually and depend on the cause : as anorexia ,nausea ,vomiting ,irritability ,muscle twitching ,increase reflexes ,convulsion , coma ,GI bleeding ,increase suseptability to infection cos decrease in immunity .
RECOVERY PHASE :
Most of the patients get better by stopping the causative insult and by giving medications to the patient but this recovery happen slowly as increase urine output and GFR and decrease in U&C .
IVx:
• Anuria suggest lower urinary tract obstruction , may complicate sever prerenal , serious GN ,vessels obstruction
• In partial urinary tract obstruction can present as polyuric .
• Prerenal uremia : urine analysis is not helpful cos there is very low renal output .
• Pigmentation (muddy brown ) characteristics of tubular necrosis , suggest ischemia or nephrotoxic .
• Red cell cast indicate glomerular insult
• White cell count interstitial nephritis .
• Broad granular cast indicate chronic renal disease
• Eosinophilic cells , in antibiotic induced allergic nephritis .
• Lymphocytes ,, indicate NSAID use .
Dx : history in
1. volume depleted : thirst ,dry mouth ,oliguria ,decrease in JVP,BP , excessive fluid loss , dry skin , postural hypertension , tachycardia .
2. volume gain : fluid overload appear as ankle odema (pitting ) ,, third heart sound , increase JVP,BP, pulmonary edema ,effusion .
urine chart in ARF :
diagnositic index prerenal interstitial renal
frac Na exam <1 >1
urine Na con <10 >20
urine cr/plasma cr >40 >20
urine ur/plasma ur >8 <3
urine specific gravity >1.018 <1.015
urine osmolarity >500 <300
plasma bun/cr ratio >20 >1
bun =blood urea nitrogen
renal function index <1 >1
Rx:
• treat the underlying cause .
• oliguric phase restrict fluid and electrolyte intake .
• restrict intake of protein to less 20g/day or stop intake if the condition is sever and instead increase the CHO intake .
• give diuretic in oliguric phase .
specific conditions treatment :
1.increase k+ level : restrict the k+ contain food , dialysis is the main treatment of k+ increase
• urgent Ca gluconate IV
• insuline intake + dextran 50% 50 ml IV ,salbutamol 0.5%-1% IV slowly or 10-20mg calcium resonium
• NaHCO3 4.2% 100mg over 5 minutes
• Dialysis is the main treatment
2.pulmonary edema :
• Oxygen with bronchodilator
• Increase the dose of diuretic till 1gm frusemide +nitroglycan 10-20mg/min
• Morphine 5mg IV
• Dialysis is the main treatment
• Sometime do venesection and take 100 ml of blood or do torniquent this is to decrease venous return .
3. metabolic acidosis :
• NaHCO3
• Dialysis
• Monitor PH and Ca level
4. hypertensive encephalopathy : Headache , check fundi ,fits , coma .
So protect the airway , and give valium for fits and if get the needed benefit use phynitoin 300mg if in coma use sodium valeproate 10mg/kg and gradual decrease in blood pressure gradually .
5. uremic encephalopathy :
• Dialysis
• Sodium valeproate ,phynitoin
6. pericarditis :
• Frequent dialysis is the best treatment
• NSAIDS to relief pain and inflammation
7. cardiac temponade : need aspiration of the fluid then frequent dialysis .
DIALYSIS : indicated in the following occasions
1. sever acidosis
2. intractable volume overload
3. increase k+level not relived by treatment
4. prophylactic in urea >100-150mg/dl or Cr level >8-10mg/dl
5. uremic encephalopathy
done by : Y.I.ZAKKO
and medicine group :
Ali Rasheed
raghad ali
farah baha
siran mahrous