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