Nephrology Flashcards
Late complication of HPP
Severe disabling proximal lower extremity weakness
Episodic weakness after 25 is still periodic paralysis
NO, Episodic weakness AFTER 25, almost never periodic paralyses, except thyrotoxic periodic paralysis
Serum Creatinine (2) and Urine Output (1) findings of Stage 1 Acute Kidney Injury
Serum Creatinine
* 1.5 to 1.9 times baseline
* >/= 0.3 mg/dL (>/= 26.5Umol/)
Urine Output
< 0.5mL/kg/hr for 6-12 hours
Serum Creatinine (1) and Urine Output (1) findings of Stage 2 Acute Kidney Injury
Serum creatinine
* 2.0 to 2.9 times baseline
Urine Output
<0.5mL/kg/hr for >/= 12 hours
Serum Creatinine (3) and Urine Output (2) findings of Stage 3 Acute Kidney Injury
Serum creatinine
* 3.0 times baseline
* Increase in serum creatinine to >/= 4.0mg/dL or >/= 353.6Umol/L)
* Initiation of RT therapy
* <18: Decrease in eGFR <35
Urine Output
* <0.3mL/kg/hr for >/= 24 hours
* Anuria >/= 12 hours
What SBP does renal autoregulation fail?
Renal autoregulation: fails once the SBP falls below 80mmHg
Cardiac output and resting oxygen received by the kidneys?
20% of cardiac output
10% of resting oxygen consumption
Definition of Acute Kidney Injury (3)
- Rise from baseline of at leats 0.3mg/dL within 48 hours
- Rise from baseline to 1.5 higher than baseline withi 1 week
- Reduction in UO <0.5mL/kg/hr longer than 6 hours
Clues suggestive of CKD
Radio: Small, shrunken kidneys with cortical thinning on renal ultrasound or evidence of renal osteodystrophy
Labs: Normocytic anemia in the absence of blood loss; Secondary hyperparathyroidism with hyperphosphatemia and hypocalcemia
Presents with Pigmented ‘muddy brown’ gradual casts and tubular epithelial cell casts
AKI from ATN d/t ischemic injury, sepsis or certain nephrotoxins
Hallmark of acute kidney injury
Elevated BUN concentration (Buildup of nitrogenous waste products)
Complications of AKI (10)
- Uremia
- Hypervolemia and Hypovolemia
- Hyponatremia
- Hyperkalemia
- Acidosis, elevation of anion gap
- Hyperphosphatemia and HypocalcemiaD-
- Bleeding
- Infections
- Cardiac complications
- Malnutrition
Only indication for fluid administration in AKI
Intavascular hypovolemia
Recommended for hypovolemic hypochloremic patients
0.9% saline
- Excessive chloride administration from 0.9% saline may lead to hyperchloremic metabolic acidosis and may impair GFR.
Definitive treatment for Hepatorenal Acute Kidney Injury
Orthotopic liver transplantation
- Bridge therapies
1. Terlipressin (a vasopressin analog), with albumin,
2. combination therapy with Octreotide (a somatostatinanalog) and Midodrine (an 21-adrenergic agonist), in combination with intravenous albumin (25–50 g, maximum 100 g/d).
Total energy intake of patients with AKI
20-30 kcal/kg/day
Protein intake of patients with noncatabolic AKI without the need for dialysis
0.8-1.0 g/kg/day
Protein intake of patients with AKI on dialysis
1.0-1.5 g/kg/day
Protein intake of patients with hypercatabolic AKI and receiving continuous RRT
Maximum of 1.7 g/kg/day
Treatment of uremic bleeding
Desmopressin and estrogen OR may require dialysis in long standing or severe uremia
Persistent UACR ___ (Male) or __ (female) on 2/3 occasions as a maker for early detection of primary kidney disease and systemic microvascular disease
> 2.5 mg / mmol (Male)
3.5 mg / mmol (female)
Component of Kidney Failure Risk (KFR) equation (5)
Age, sex, region (North America vs Non-North America), GFR and UACR
Predict risk of progression to stage 5 dialysis-dependent kidney disease
Indications for referral to nephrologist in patients with CKD stage 3 and 4 (3)
- Declining GFR
- Albuminuria
- Uncontrolled hypertension
Leading categories of etiologies of CKD (5)
Diabetic nephropathy
GN
HTN-associated CKD
ADPKD
Other cystic and tubulointerstitial nephropathy