CKD Flashcards by Kyra Porter

chronic kidney disease (CKD) - defined

*defined by 3 or more months of:
-kidney damage
OR
-decreased kidney function

How well did you know this?

Not at all

Perfectly

chronic kidney disease (CKD) - etiologies

glomerular diseases:
-DIABETES, autoimmune diseases, systemic infections, drugs, neoplasias
vascular diseases:
-atherosclerosis, HTN, ischemia, vasculitis, thrombotic microangiopathy
tubulointerstitial diseases:
-chronic UTIs, stones, obstruction, drug toxicity
cystic diseases:
-polycystic kidney disease

How well did you know this?

Not at all

Perfectly

decreased kidney function

*GFR is best overall index of kidney function for healthy individuals & those with CKD
*GFR = sum of the filtration rates in all of the functioning nephrons
*healthy glomeruli collectively filter 180 liters per day
*normal GFR in healthy young adults ~125 mL/min
*GFR < 15 mL/min is defined as kidney failure

How well did you know this?

Not at all

Perfectly

measured GFR

*measurement of ideal urinary clearance filtration markers
*gold standard is inulin or lothalmate

How well did you know this?

Not at all

Perfectly

estimated GFR

*serum biomarkers input to complex equations to approximate the true GFR
*this is routinely done in clinical practice
*note that all of the equations for eGFR have limitations

How well did you know this?

Not at all

Perfectly

chronic kidney disease (CKD) due to kidney damage - defined

*preserved GFR
*histopathological abnormalities
*abnormalities in serum/urine tests or abnormalities on imaging that may lead to a drop in GFR (e.g. albuminuria, polycystic kidney disease)

How well did you know this?

Not at all

Perfectly

chronic kidney disease (CKD) due to decreased kidney function - defined

*drop in GFR (GFR < 60 mL/min per 1.73 m^2)
*with or without kidney damage

How well did you know this?

Not at all

Perfectly

stage I chronic kidney disease (CKD)

*kidney damage with normal or increased GFR
*GFR > 90

How well did you know this?

Not at all

Perfectly

stage II chronic kidney disease (CKD)

*kidney damage with mild decreased GFR
*GFR 60-89

How well did you know this?

Not at all

Perfectly

stage III chronic kidney disease (CKD)

*moderately decreased GFR
*GFR 30-59

How well did you know this?

Not at all

Perfectly

stage IV chronic kidney disease (CKD)

*severely decreased GFR
*GFR 15-29

How well did you know this?

Not at all

Perfectly

stage V chronic kidney disease (CKD)

*kidney failure
*GFR < 15 (or dialysis)

How well did you know this?

Not at all

Perfectly

who should be screened for CKD?

*all patients who have increased susceptibility or have potential inciting factors should be screened for CKD
*most screening is done with serum creatinine based estimating equations

How well did you know this?

Not at all

Perfectly

CKD progression

*chronic kidney disease is often PROGRESSIVE and leads to IRREVERSIBLE loss of renal function
*once GFR falls below about 50% of normal, kidney function tends to continually decline, even if the initial insult has been eliminated

How well did you know this?

Not at all

Perfectly

adaptive hyperfiltration

*a compensatory process in which the kidneys adapt to the initial damage by increasing the filtration rate in the normal (undamaged) nephrons
*results in long-term damage to the remaining nephrons
*manifested by more proteinuria and progressive CKD

How well did you know this?

Not at all

Perfectly

effects of proteinuria in chronic kidney disease (CKD)

*proteinuria itself contributes to progressive nephron damage
*excessive tubular reabsorption → protein overload; the reabsorbed tubular proteins signal pro-inflammatory mediators and macrophage recruitment
*complement activation → alterations of cytoskeleton, production of ROS, & synthesis of more pro-inflammatory mediators
*inflammation → accumulation of ECM collagen, fibronectin, and other components → interstitial fibrosis

SGLT2 inhibitors in CKD

*SGLT2 inhibitors block reabsorption of glucose in the proximal tubule
*lowers the renal glucose threshold → substantial glycosuria (increased release of glucose in the urine)
*also have effects independent of glycemic control

risk factors for progression of CKD

*PROTEINURIA!!!
*hypertension
*type of underlying disease (diabetes, PKD)
*African American ancestry
*male gender
*obesity
*smoking
*high protein diet
*phosphate retention
*metabolic acidosis

mainstays of CKD management to slow progression

treat the underlying cause, if possible
address modifiable risk factors (correct HTN, initiate statin therapy, encourage smoking cessation, use ACEi or ARB + SGLT2 inhibitor)
prepare for renal replacement therapy (RRT = dialysis) or transplant

medical complications of CKD

*HTN
*cardiovascular disease
*anemia
*secondary hyperparathyroidism
*metabolic acidosis
*dyslipidemia
*uremia

pathogenesis of CKD → HTN

sodium retention: Na+/H2O balance disrupted as GFR declines
increased activation of RAAS: prob due to regional ischemia & scarring
enhanced activity of sympathetic nervous system
secondary hyperparathyroidism: rise in intracellular calcium → vasoconstriction
impaired nitric oxide synthesis & endothelium-mediated vasodilation

why is HTN an important complication of CKD?

*HTN is an independent risk factor for cardiovascular disease (CVD)
*each increment of 20/10 mmHg above 115/75 doubles your risk of a cardiovascular event
*CVD is the leading cause of death in patients with CKD

treatment of HTN when diabetes or CKD present

*goal is < 140/90
*initiate ACEi or ARB +/- SGLT2 inhibitors

*purpose: slow progression of CKD and reduce rate of cardiovascular complications

pathogenesis of CKD → anemia

*CKD results in decreased EPO (erythropoietin) from peritubular cells
*as GFR decreases, anemia is more severe

*other causes include:
-absolute of functional iron delivery
-shortened RBC survival (esp dialysis pts)
-blood loss due to uremic platelet dysfunction
-nutritional deficiencies
-inflammation
-ACEi use

treatment of anemia in pts with CKD

*exclude non-renal causes of anemia (GI blood loss, B12 deficiency, etc) *correct iron deficiency (oral or IV iron supplementation) *initiate erythrocyte stimulating agents (ESA) - recombinant human EPO note - generally do not treat to a Hb > 12-13

pathogenesis of CKD → secondary hyperparathyroidism

1. decreased GFR → substantial **increases in phosphate retention** 2. **FGF-23 increases to improve renal phosphate clearance (increase excretion of phosphate)** 3. high FGF-23 levels suppress 1,25 Vitamin D activity 4. low vitamin D activity → HYPOCALCEMIA 5. **PTH secretion increases to maintain normocalcemia** 6. clinically apparent rise in phosphorous is a very late finding

complications of secondary hyperparathyroidism due to CKD

1. mineral bone disease → renal osteodystrophy → increased risk of fractures, esp hip fractures → increase in mortality 2. soft tissue and extra-skeletal calcifications (in coronary or peripheral arteries, skin or soft tissue [calciphylaxis])

treatment of secondary hyperparathyroidism in CKD pts

*control serum phosphate levels *control metabolic acidosis *suppress PTH levels (active oral vitamin D supplementation - calcitriol) *consider subtotal parathyroidectomy

pathogenesis of CKD → metabolic acidosis

*increasing **tendency to retain hydrogen ions** in patients with CKD *leads to **progressive metabolic acidosis** *consequences: increased bone resorption, enhances protein catabolism, contributing to malnutrition

treatment of metabolic acidosis in CKD pts

*oral bicarbonate supplementation

pathogenesis of CKD → dyslipidemia

*abnormal lipid metabolism is common in patients with renal disease/CKD *initiate statin therapy to treat

pathogenesis of CKD → uremia

*uremia: clinical syndrome attributed to accumulation of uremic toxins (we often use UREA as a marker) *associated with ADVANCED CKD (stage V) *symptoms: fatigue, pruritus, dysgeusia, anorexia, nausea, vomiting, restless legs *signs: serositis, pericarditis, asterixis, skin changes, weight loss/malnutrition, platelet dysfunction, peripheral neuropathy

treatment for uremia in advanced CKD pts

*renal replacement therapies (dialysis or transplant)