Renal: Lecture 3 Flashcards
Where do nephrons live in kidney?
Medulla and Cortex
Drain into renal pelvic
Inactive form of vitamin D
25 (OH) - D
Active form of Vitamin D
1,25 (OH)2D
Proposed mechanisms for CKD progression
Diabetes mellitus
Systemic Hypertension
Glomerulosclerosis
How do we get CKD from Systemic Hypertension
Increase in glomerular capillary pressure
Thickening of blood vessels, reducing blood flow, leading to decreased perfusion, so body will activate RAAS to try to address and makes it all worse
How do we get CKD from Diabetes mellitus
High glucose = high glucose in urine causing damage in cells. Causes scaring, Mesangial cells will expand pushing on blood vessels to constrict them.
High glucose can also lead to oxidative stress leading to dec GFR and loss of nephron
How do we get CKD from Glomerulosclerosis
Scar tissue is developed in Glomerulus
Hypertension CKD Pathogenesis
Hypertension leads to thickening and narrowing of artery and afferent arteriole.
Decrease in GFR, causes Renin secretion and Activation of RAAS.
RAAS leads to more hypertension
Modifiable CKD Risk factors
*Diabetes
*Hypertension
Hyperlipiddemia
Tobacco use
Proteinuria
History of AKI
Non-modifiable CKD Risk factors
Age 60+
FH of kidney disease
Ethnicity: AA, Hispanic, Asian, American Indian
Common causes of CKD
- Hypertension
- Diabetes
Acute kidney injury
Polycystic kidney disease
Other (Meds, etc)
Physical Signs of CKD
Swelling/Edema Back pain Blod in urine Decreased urine output Frothiness of urine ** Usually Asymptomatic, Especially early stage**
Labs present for CKD
Either of these must be present for >3 months
eGFR <60
UACR >30
Markers of kidney damage (1 or more0
Markers of Kidney Damage
Urinalysis abnormalities
Kidney biopsy abnormalities
Polycystic kidney disease on imaging studies
Differences between AKI and CKD
AKI: Short time frame, Double in SCr
CKD: Over prolonged period of time, dec eGFR and inc UACR
GFR gives estimation of….
function and filtration
UACR provides info regarding
Extent of kidney damage