Chronic Kidney Disease Flashcards
define CKD
chronic kidney disease
irreversible progressive loss of kidney function over a min 3M period
what is the KDIGO CKD classification categories
Stage 1: eGFR >90 AND evidence of kidney damage
Stage 2: eGFR 60-89 AND evidence of kidney damage
Stage 3a: eGFR 45-59
Stage 3b: eGFR 30-44
Stage 4: eGFR 15-29
Stage 5: eGFR <15 or on dialysis ➔ end-stage renal disease (ESRD)
can CKD be reversed?
No, goal of care is slowing down damage
T/F: cardiovascular disease is the leading cause of death in CKD pts
True!
most patients end up passing from an MI, not from their actual CKD
what are 4 non-modifiable RF for CKD?
- Older age (>60Y)
- Male gender
- Non-white ethnicity → African Americans, Afro-Caribbean individuals
- Some genetic factors → polymorphisms
what are some modifiable RFs (name 3) for CKD that increase the rate of CKD progression?
- systemic HTN
- proteinuria ➔ seen mostly in diabetic nephropathy
- metabolic factors ➔ obesity, smoking, insulin resistance, dyslipidemia
what are the two most common causes of CKD?
DM (mostly T2DM) and HTN
Besides DM and HTN, what are 3 other causes of CKD?
- nephrotic syndrome
- nephritic syndrome
- hereditary or cystic diseases (polycystic kidney disease)
- neoplasms ➔ w/ mass effect on kidneys
- NSAIDs and lithium
- infections
- Atherosclerosis
pathophys of CKD with HTN as cause
- Increased systemic BP
- increased blood volume to renal arteries
- Hypertrophy of the vasculature to compensate for increase stretch –> Over time → thickening of the membrane → narrowing of lumen + decreased flexibility of the artery
- Decreases blood flow through afferent arteriole → decreases GFR
- Decreased GFR signals to juxtaglomerular cells, release renin → active RAAS
- Perpetuates high BP and continues to damage the afferent arteriole
- Decreased perfusion to the glomerulus → ischemic injury → glomerulosclerosis
- Ischemia to tubules → tubular atrophy → chronic interstitial nephritis
Net: nephron loss → gradual decline in GFR
pathophys of CKD with DM as cause
- glycosylation of efferent arteriole –> sclerosis
- blood pooling in glomerulus –> increases eGFR
- more sugar getting filtered into nephron
- more glucose + Na reabsorbed at SGLT2
- macula densa thinks low GFR bc low Na at distal convulated tubule
- activates RAAS to try to increase eGFR
- results in HTN –> hypertrophy of arterioles –> decrease blood flow –> ischemia –> nephron loss and decline in GFR
T/F: stages 1-3 of CKD typically do not have symptoms of CKD
True! symptoms of CKD usually start appearing in stages 4/5
however they may have s/s of their underlying cause
how might a patient present (s/s) if they have stage 4/5 CKD
May present with
- generalized edema
- shortness of breath
- anemia s/s bc decreased EPO synth from kidney
- weight loss
- urinary: oliguria
- mineral and bone disorder s/s (bone pain/fractures)
- malaise, palpitations, arrhythmias from hyperkalemia
- uremia associated s/s (bleeding and ecchymosis, pericarditis, encephalopathy)
- generalized: N/V, loss of appetite, HTN, persistent pruritus, sleep disturbances
explain anemia in CKD pts
- kidney damage ➔ decreased EPO ➔ less RBC produced ➔ anemia
- poor kidney function ➔ decreased kidney filtration function ➔ accumulation of toxins ➔ decreased lifespan of RBC
explain how CKD pts can have metabolic acidosis
kidney can acidify urine but produce less ammonia → cannot excrete adequate H+
bicarb and ammonia are produced in the same reaction in the proximal tubule
so if there is less ammonia production then there is less bicarb production as well which contributes to metabolic acidosis
explain how renal osteodystrophy occurs in CKD
disturbed calcium and phosphate homeostasis due to kidney injury
- The kidney’s ability to excrete phosphate decreases ➔ hyperphosphatemia
- high phosphate ➔ binds up any free calcium ➔ calcium phosphate
- kidney damage also decreases ability to activate vitamin D to be able to absorb calcium from GI tract
- decreased amount of serum ionized calcium ➔ stimulates PTH release
- 2ndard hyperparathyroidism ➔ maladaptive high bone turnover
- results in poor bone healing/bone pain + parathyroid hyperplasia (tertiary hyperparathyroidism) + extraosseous calcifications (of soft tissues and vasculature)
how is osteodystrophy and atherosclerosis related in CKD?
osteodystrophy can result in calcification and stiffening of the blood vessels ➔ atherosclerotic disease
how does CKD, albumin, and atherosclerotic disease relate to one another
CKD ➔ kidney damaged ➔ increased permeability of the glomerular filtration barrier ➔ increased excretion of albumin ➔ hypoalbuminism ➔ stimulates liver synthesis ➔ increased triglycerides ➔ atherosclerotic disease s/s like angina, chest pain, and dyspnea/SOB
what physical exams should be done to evaluate a CKD pt?
- volume status ➔ edema, pulses, ascites, cyanosis, pallor, JVP
- vitals ➔ BP (HTN)
- resp ➔ crackles
- cardio ➔ extra heart sounds
- CVA tenderness ➔ most likely negative
- diabetic screen ➔ retinopathy, foot exam, wound healing
what ix could you order for CKD?
- urine dipstick (proteins, blood)
- urine albumin: creatinine ratio
- creatinine, urea
- serum albumin
- lipid panel (LDL, HDL, TG, TC)
- CBC - anemia
- electrolytes and extended electrolytes
- EPO
- Imaging: U/S kidney, if obstructive presenting, consider CT
- w/u for DM - A1c and POC glucose
- tests to determine etiology (autoimmune like ANA, hepatitis serology, HIV serology, biopsy)
what ix is diagnostic for CKD?
- creatinine ➔ eGFR
- urine albumin:creatinine ratio
what ix should always be ordered for monitoring visits for CKD?
Creatinines and urine albumin:creatinine ratios
monitor any cx the pts has
how do you manage CKD pts?
- tx underlying cause of CKD if identified
- all pts get ACEi/ARB even if not HTNive
- HTN: ACEi/ARB
- DM: SGLT2i and metformin - primary prevention of ASCVD: statins (1st line), ASA (2nd)
- re: mineral and bone s/s: vitamin D and calcium
- pt education: diet, exercise, smoking cessation
- consider dialysis or transplant if eGFR <30 (stage 4/5), refer to nephro
