Chronic Kidney Disease Flashcards
what are the functions of the kidneys
- excretory
- endocrine
- regulatory
how do changes in cardiac output affect the kidneys
kidneys receive 25% of CO - reduction in CO severely affects the kidneys
what is a nephron
functional unit of the kidney
glomerular filtration rate
filtration rate of all functioning glomeruli
- depends on the proportion of perfused and filtering glomeruli
single nephron GFR x total # of nephrons
what are reserve glomeruli
“backup” nephrons that are non-perfused in health
become perfused when normal ones get damaged
how does chronic kidney disease develop
damage and loss of functional nephrons –> recruitment of reserve nephrons –> loss of critical mass (all reserve nephrons are used up) –> hyperperfusion and hyperfiltration of surviving nephrons –> overwhelms remaining nephrons –> glomerular hypertension –> inflammation and progressive damage –> CKD
interstitium gets replaced with fibrosis
what is renal failure
failure of the kidneys to carry out their normal functions –> accumulation of uremic toxins and dysregulation of fluid, electrolyte, and acid-base balance
when can a diagnosis of chronic kidney disease be made
irreversible + progressive structural/functional abnormalities in the kidneys that persist for > or = 3 months
can only SLOW progression - can NOT reverse it
can a patient have CKD without being azotemic
YES - must lose 70-75% of renal functional mass in order for creatinine to exceed the reference interval
have to monitor increasing trends in creatinine in order to detect CKD before azotemia develops
how can a diagnosis of CKD be made
increasing creatinine with inappropriate urine concentration
usually isosthenuria with dehydration
ALWAYS evaluate alongside comorbidities, fluid administration, and medication
what must always be done before a diagnosis of CKD can be made
rule out all causes of acute kidney injury
- pyelonephritis, ureteral obstruction, leptospirosis, nephrotoxins
confirm the damage is IRREVERSIBLE before diagnosing
chronic kidney disease general disease presentation
long history of illness
thin BCS + history of weight loss
anemia
normal to small/irregular kidneys
at what % nephron loss does creatinine exceed reference interval
70-75%
what is the best way to interpret creatinine
monitor trends
do NOT just look at reference interval
creatinine in small vs large breeds
small: lower creatinine (0.5-0.9)
large: higher creatinine (0.7-1.8)
at what % nephron loss does SDMA exceed reference interval
40%
always evaluate alongside creatinine, BUN, and USG
best used in patients with normal creatinine + isosthenuria
what steps should be taken if a patient has an elevated SDMA + normal creatinine
can start taking renal precautions in terms of diet, drug use/disuse, and monitoring
stage 1 CKD
“non-azotemic” CKD
creatinine within reference interval BUT patient is showing signs of renal dysfunction (inability to concentrate urine, renal abnormalities on US, increasing creatinine trends, renal proteinuria)
CKD substaging
move up 1 stage if proteinuria or hypertension
clinical signs of CKD
appear around stage 2
- PU/PD
- weight loss
- GI signs
- lethargy, inappetance
- oral ulcers (uremic toxins)
clinical consequences of CKD
- uremic stomatitis
- uremic gastropathy
- anemia
- dehydration
- hypertension
- hypokalemia
- metabolic acidosis
- hyperphosphatemia
9.low calcitriol
when should a patient be treated for uremic gastropathy
only if showing signs of GI bleeds - hematemesis, melena, etc
what causes anemia with CKD
- GI hemorrhage
- iron deficiency
- decreased EPO
how to treat iron deficiency
ensure adequate nutrition
iron dextran injection
how to treat anemia due to decreased EPO
erythropoiesis stimulating agents (ESAs)
- darbepoetin (aranesp)
molidustat - promotes erythropoiesis by increasing endogenous EPO + increases iron availability
always ensure adequate iron load prior to administration
when should IV/SQ fluids be used in CKD patients
ONLY in order to prevent or treat hydration
ex. if patient is dehydrated OR if patient is hydrated but has ongoing losses (vomiting, diarrhea)
what causes hypertension with CKD
renal dysfunction leading to decreased BP regulation by kidneys
outcomes of hypertension
- progressive renal damage
- retinal detachment
- CV effects (LV hypertrophy)
- hypertensive encephalopathy
hypertension treatment
amlodipine
ACE inhibitors
angiotensin receptor blockers (ARBs)
how does hypokalemia occur with CKD
malnutrition/decreased intake
exacerbated by renal losses and malabsorption
treatment for hypokalemia
- ensure adequate nutrition
- potassium gluconate (tumil K)
how does CKD cause a metabolic acidosis
accumulation of uremic acids AND inability to produce bicarbonate
treating metabolic acidosis
before treating, ALWAYS correct:
1. dehydration (need to correct underlying lactic acidosis)
2. hypokalemia (sodium bicarb will exacerbate hypokalemia)
treatment: sodium bicarbonate
what is the ideal sodium bicarbonate levels
20 mmol/L
how to calculate bicarbonate deficit
bicarb deficit = BW (kg) x base deficit x 0.3
base deficit = 20 - current bicarbonate
how does CKD cause hyperphosphatemia
phosphorus retention in the kidneys
leads to secondary renal hyperparathyroidism + tissue mineralization
pathogenesis of renal secondary hyperparathyroidism
high P –> complexes with Ca in tissues –> decreases iCa in serum –> low Ca stimulates PTH –> PTH causes increased Ca and stimulates P excretion –> P unable to be excreted due to CKD –> hypercalcemia + hyperphosphatemia
treatment for hyperphosphatemia
low phosphate diet
phosphate binders
what causes low calcitriol in CKD
renal secondary hyperparathyroidism
elevated PTH should stimulate calcitriol activation in the kidneys BUT kidneys are dysfunctional –> decreased active vitamin D –> exacerbates renal secondary hyperparathyroidism
NO standard treatment
general CKD management
- hydration - IV or SQ fluids only if indicated
- nutrition - renal diets, appetite stimulants if severely ill, enteral feeding tube
what is the overall goal of nutritional CKD management
- adequate calories (meet energy requirements)
- alleviate clinical signs
- minimize electrolyte, acid-base, and fluid abnormalities
- slow disease progression
how to ensure adequate calories
monitor appetite due to waxing/waning appetites of CKD patients
want to ensure patient is eating diet, if not may need to consider switching diet or enteral feeding tubes
CKD diet parameters to improve clinical signs
LOW protein
MAINTAIN sodium
HIGH potassium, bicarbonate, B vitamins
CKD diet parameters to slow progression
LOW phosphorus, protein
HIGH omega 3 FAs, antioxidants
what stages of CKD is it most important to reduce dietary protein
stages III-IV
lowering protein reduces uremia
what renal disease is it most important to reduce dietary protein
PLNs (protein losing nephropathies)
protein will worsen renal tubular damage
low protein will decrease glomerular hypertension
dietary sodium goals for CKD
0.4-1.5 g per 1000kcal
do not want too low - will stimulate RAAS
do not want too high - will increase risk of hypertension
why is it important to supplement potassium in CKD diets
high risk of hypokalemia in CKD
why is it important to supplement HCO3 in CKD diets
want to alkalinize the urine to combat metabolic acidosis
how does reducing phosphorus help in CKD
controls PTH levels + reduces risk of soft tissue mineralization
increased P can cause kidney injury
important dietary considerations
- do not switch during stress, illness, or hospitalization
- switch diet gradually
- ensure adequate water intake
- may need to rotate or add variability for palatability
what parameters should be monitored in CKD patients
- appetite
- weight trends
- muscle mass trends
- azotemia
- phosphorus
- electrolyte imbalances
- serum albumin/UPC
