Proteinuria, Oliguria and Polyuria Flashcards
Anuria
UOP <50-100 ml/day
Oliguria
UOP <400-500 ml/day
Polyuria
UOP >3000 ml/day
Azotemia
Elevated BUN without symptoms
Uremia
Elevated BUN w/ symptoms such as:
- N/V
- Confusion
- Pruritus
- Metallic Taste
- Fatigue
- Anorexia
CKD Criteria
- Markers of Kidney damage: Albuminuria, increased urine sediment, electrolyte/Renal Tubular disorder, kidney transplant
- Decreased GFR <60 ml/min/1.73m^2
Either or both for minimum 3 months
How would you distinguish CKD from AKI?
Time of symptoms:
<3 months= AKI
>3months= CKD
Briefly describe the stages of CKD
1-5: 1 is mild with >90 GFR; 5 is ESRD with <15 GFR
If GFR is between 60-90 (stage 1-2) but no symptoms, it’s not CKD
Top 4 RF for CKD
- DM
- HTN
- CVD
- AKI
Notable: NSAID use, Age>65, AA population
Clinical presentation of CKD
Edema HTN Oliguria/Anuria Proteinuria Uremia Asterixis Uremic Frost
3 tests to identify CKD
- eGFR
- Urine Albumin:Creatinine Ratio or PRO:Creatinine Ratio
- Urinalysis
What U/S findings are indicative of CKD?
Atrophic/small kidneys (normal= fist)
Cortical thinning (normal= >1cm)
Increased echogenicity
Elevated resistive index (renal artery stenosis)
Indications for dialysis
AEIOU: Acidosis Electrolyte disturbance Ingestion of toxins (GOLDMARK and ME DIE) Overload volume Uremia
2 tests to determine AKI
Serum Creatinine- increased
Urine Output- decreased
do not need to memorize stages, but know that Serum creatinine 1.5-1.9x starts and/or UO <0.5ml/kg/h starts stage 1
Common causes of prerenal AKI
Hypotension
Hypovolemia
Reduced CO (HF)
Systemic vasodilation (sepsis)
Causes of Postrenal AKI
Any obstruction
What causes 85% of intrinsic AKI
ATN- ischemic or toxic
What labs should you obtain on ALL AKI patients?
Urinalysis with microscopy
Urine albumin:creatinine ratio or pro:creatinine ratio
How can FeNa help determine cause of AKI?
FeNa<1% is prerenal
FeNa>2% is ATN (intrinsic)
When is FeUrea used over FeNa?
In patients on diuretics/fluids
Urine Microscopy findings in ATN
epithelial cells, granular casts, waxy casts
Urine Microscopy findings in AIN
WBC/WBC casts, eosinophils
Complications associated with AKI
Hypervolemia
Electrolyte imbalance
Hyperuricemia
Acidosis
Nephrotic syndrome definition
Proteinuria >3.5 g/day Hypoalbuminemia Edema Hyperlipidemia Lipiduria
Important pathogenic cause of Nephrotic syndrome
Low renal perfusion leads to over activation of RAAS and increased Na+ and H2O retention
Nephrotic Syndrome Ddx
- Diabetic Nephropathy
- Minimal Change Dz (children)
- FSGS (adults and some children)
- Membranous Nephropathy (adults)
Nephritic Syndrome definition
Proteinuria <3.5 g/day
Hematuria
HTN
Active urinary sediment (RBC and casts)
Nephritic Syndrome Ddx
- IgA nephropathy
- Thin BM Nephropathy
- MPGN
- Lupus Nephritis
- RPGN
- APGN (post-infectious)
What labs would you order???
Just wanted to put in here that I’m sure we’ll get questions that lead us to a diagnosis and then ask what lab test to order.
For example: Pt looks like they have FSGS and are sexually active, order and HIV test
Describe the 2 types of Diabetes Insipidus
- Central- lack of ADH in circulation. Corrects with administration of Vasopressin.
- Nephrogenic- lack of response to ADH. Does NOT correct with Vasopressin.
MoA of ADH
Binds V2R on basolateral collecting duct cell and increases cAMP which drives insertion of AQP2 and Urea channels on apical membrane.
Effect: Increased Water resorption & urea (BUN:creatinine increased)
Allison is prescribed Lithium because she’s unhinged. What can this possibly lead to?
Nephrogenic Diabetes Insipidus due to increased degradation of AQP2 channels.
How does Calcium levels affect resorption?
Hypercalcemia leads to activation of Ca-sensor on basolateral membrane of TAL. This inhibits ROM-K channel which decreased NKCC2.
Similar to loop diuretic and Bartter Syndrome
Explain results of Water Deprivation test for central and nephrogenic Diabetes Insipidus
Central: low urine osmolality that corrects with ADH
Nephrogenic: low urine osmolality that does not correct
Normal person: high urine osmolality that does not change with ADH administration.
Treatment for Nephrogenic DI
Decrease solute intake
Thiazide diuretic
NSAIDs (inhibit PG’s because PG’s inhibit ADH)