Acute Kidney Injury by Osama El-Mishawy,MD Head of ...
Transcript of Acute Kidney Injury by Osama El-Mishawy,MD Head of ...
Acute Kidney Injury
by
Osama El-Mishawy,MD
Head of Medicine & Nephrology
Case Study F.J. 63 year old female with a 15 year diagnosis of DM, presents in
the clinic.
She also has a 10 year history of HTN.
Her DM & HTN has been only moderately controlled. Today she reports edema in her hands, face, and feet. She reports that she is tired and "just doesn't seem to have any energy". Her blood sugar is within acceptable limits. Her urine is positive for blood and protein. What complication of diabetes might you suspect?
A-Ureteral Epispadias.
B-Wilms Tumor.
C-Chronic kidney failure related to diabetic nephropathy.
D-Acute renal failure related to a severe urinary tract infection.
Case Study Frances Jenkins, 63 year old female with a 15 year diagnosis of
Diabetes, presents in the clinic. She also has a 10 year history of hypertension. Her diabetes and hypertension has been only moderately controlled. Today she reports edema in her hands, face, and feet. She reports that she is tired and "just doesn't seem to have any energy". Her blood sugar is within acceptable limits. Her urine is positive for blood and protein.What complication of diabetes might you suspect?
A-Ureteral Epispadias.
B-Wilms Tumor.
C-Chronic kidney failure related to diabetic nephropathy.
D-Acute renal failure related to a severe urinary tract infection.
Case Study
S.M. a 19 year old student, was badly injured in a MVA a few days ago in a rural location. He was trapped in the vehicle for over an hour and transported to the ER approximately 2 hours after he sustained injuries. He is in intensive care with a fractured pelvis, femur, ribs, and shoulder. He also suffered a tension pneumothorax and a head injury. He was in shock when he arrived in the ER. His BP has remained somewhat low despite fluids and medication. His hourly urinary output has gradually declined. What pathophysiological process should you be concerned about at this point?
A-Neurotoxicity of medications.
B-Liver failure.
C-Acute renal failure.
D-Renal calculi.
Case Study
S.M. a 19 year old student, was badly injured in a MVA a few days ago in a rural location. He was trapped in the vehicle for over an hour and transported to the ER approximately 2 hours after he sustained injuries. He is in intensive care with a fractured pelvis, femur, ribs, and shoulder. He also suffered a tension pneumothorax and a head injury. He was in shock when he arrived in the ER. His BP has remained somewhat low despite fluids and medication. His hourly urinary output has gradually declined. What pathophysiological process should you be concerned about at this point?
A-Neurotoxicity of medications.
B-Liver failure.
C-Acute renal failure.
D-Renal calculi.
Differentiating ARF vs. CRF
1) History
2) Oliguria = ARF; acute CRF decomposition
3) Renal ultrasound
Normal or large = acute
small = CRF (unless PKD, diabetes, amyloid)
4) ARF =Unstable azotemia
5) Anemia – unreliable for ARF vs. CRF
6) Urinalysis –normal suggesting pre-renal azotemia
Pre-Renal Azotemia
Definition:
A reduction in glomerular filtration rate (GFR) due to a ↓ glomerular capillary pressure
Diagnosis:
Characteristic clinical setting and urinary findings
Response to the correction of the pre-renal state
Pre-Renal Azotemia: Causes
1) ↓ cardiac output
CHF
Intravascular volume depletion
2) Normal Cardiac Output
Selective renal vasoconstriction (NSAIDS,)
Hepatorenal syndrome
Pre-Renal Azotemia: Renal
Manifestations
1) Relatively normal urinalysis
2) Relatively normal serum bicarbonate
3) High BUN/creatinine ratio
4) High urine osmolality (typically >600 mosm/kg)
Hepatorenal Syndrome (HRS)
Definition:
“Irreversible” pre-renal azotemia in the setting of end-stage hepatic disease
Pathogenesis:
1) renal vasoconstriction induced by unknown mediators
2) Renin/angiotensis, endothelin, NO, endotoxin,
↑sympathetic tone all implicated; none proven and may reflect secondary phenomena
HRS: Differential Diagnosis
1) Rule out volume depletion by volume challenge
2) Rule out combined hepatic and renal epithelial
injury
3) Rule out ATN (which is common in the HRS patients)
HRS: Therapy 1) Portal-systemic shunts: acute, but not long term
benefits
2) Paracentesis: no proven benefit; may precipitate ARF
3) Vasodilator therapy: no proven benefit
4) Dialysis:
IF a possibility of hepatic functional recovery
IF there is a likelihood of ATN (high urine Na)
5) Hepatic transplantation
Obstructive Nephropathy
1) Incidence: ≈ 5-10% ARF cases
2) Causes:
Children: anatomic (urethral valves, ureteral-vesical or
ureteral-pelvic stenosis)
Young adults: stones; retroperitoneal processes (tumor,
infections)
Elderly: GU tumors (bladder, cervical); BPH
Obstructive Nephropathy 3) Symptoms:
• Pain, common if acute:
• Abnormal urine flow – absolute anuria (acute GN,
cortical necrosis), oliguria, or nonoliguria
• Hematuria
Thank you