CKD - amboss Flashcards
define CKD
abnormality of kidney structure of function that persists > 3 months
common causes include diabetes, hypertension, and glomerulonephritis
pathos of diabetic nephropathy
hyperglycaemia causes varying degrees of damage to all types of kidney cells
pathos of hypertensive nephropathy
caused by protective autoregulatory vasoconstriction of preglomerular vessels
benign nephrosclerosis (sclerosis of afferent arterioles and small arteries
decreased perfusion
ischaaemic damage
pathos of glomerulonephritis
noninflammatory GN eg. membranous nephropathy, focal segmantal glomerulosclerosis
inflammatory GN eg. lupus nephritis, post streptococcal GN, rapid progressive GN, haemolutic uraemic syndrome
pathophys of CKD
reduced GFR causes decreased production of urine which leads to increase in extracellular fluid volume and total body volume overload
decrease in excretion of waste products eg. urea, drugs
decrease in excretion of phosphate causes hyperphosphataemia
decreased maintenance of acid base balance leads to metabolic acidosis
decrease in maintenance of electrolyte concentration causes electrolyte imabalances eg. Na retention
reduced endocrine activity in CKD
decrease in hydroxylation of calcifediol causes decreased production of calcitriol - decreased serum Ca
decreased in erythropoetin excretion causes decreased stimulation of erythropoiesis
reduced gluconeogenesis causes increased risk of hypoglycaemia
clinical features of CKD
patients are often asymptomatic until later stages due to the exceptional compensatory mechanisms of the kidneys
hypertension, heart failure, pulmonary oedema and peripheral oedema due to Na and H2O retention
define uraemia
accumulation of toxic substances due to decreased renal excretion. These toxic substances are mostly metabolites of proteins such as urea, creatinine, β2 microglobulin, and parathyroid hormone.
uremia symtpoms
constitutional: fatigue, weakness, headaches
GI symptoms: nausea and vomiting, loss of appetite, ammonia breath
derm: pruritis, skin colour changes, uremic frost
serositis: uremic pericarditis, pluritis
neuro: asterixis, uremic encephalopathy, peripheral neuropathy
haematologic: anaemia, leukocyte dysfunction, increased bleeding tendancy
uremic fetor
characteristic ammonia or urine like breath odour
uremic frost
uraemia leads to high levels of urea excreted in the sweat, the evaporation of which results in yellow white urea deposits on the skin
serositis
An inflammation of any serous surface such as the pericardium, pleura, or peritoneum. Usually associated with autoimmune diseases, such as systemic lupus erythematosus and rheumatoid arthritis.
uraemic pericarditis
complicaation of chronic kidney disease that causes fibrinous pericarditis
clinical features include chest pain worsened by inhalation
physical examination findings include friction rub on auscultation, ECG changes that would normlly be seen in non uremic pericarditis are not usually seen
signs of uraemic encephalopathy
seizures
somnolence
coma
criteria for chronic kidney disease
GFR < 60 for 3 months
define end stage renal disease
irreversible kidney dysfunction with GFR < 15 mL
manifesttions of uraemia requiring chronic renal transplant therapy with either dialysis or renal transplantation
likely death by cardiovascular disease
how do people with end stage renal disease usually die
Most likely due to associated complications (e.g., anemia of chronic kidney disease) and increased cardiovascular risk factors (e.g., hypertension)
CGA classification of chronic kidney disease
classified according to GFR and albuminuria
higher stages correlate with poorer prognosis
determining albuminuria category
Spot UACR: The ratio of urine albumin concentration to urine creatinine concentration. An ACR < 30 mg/g is considered normal to mildly increased; an ACR 30-300 mg/g for more than 3 months indicates likely chronic kidney disease. An ACR > 300 mg/g is severely increased.
other urine studies for CKD
Spot UPCR: The ratio of total protein to total creatinine in the urine. The UPCR obtained from a single urinary sample (i.e., spot urine) can be used to estimate 24-hour protein excretion (assuming creatinine is excreted at a constant rate). A spot UPCR value typically approximates the number of grams of protein excreted in the urine in a 24-hour period (e.g., a spot UPCR of 3.0 can be used to estimate proteinuria of ~ 3.5 g/day).
urine dipstick: may show hematuria or proteinuria
urine microscopy: may show abnormal urine sediment
US of kidneys and urinary tract
first line imaging technique for the assessment of kidney structure
conider obtaining for all patients to further support the diagnosis and help determine the etiology
findings on US suggesting chronic kidney disease
decrease in kidney length <10cm
decrease in parenchymal and/or cortical thickness
increase in cortical echogenicity
cysts
califications
findings on US that suggests specific aetiologies
ureteral or renal pelvic dilation suggests obstructive nephropathy
bilaterally enlarged kidneys with multiple cysts suggest polycystic kidney disease
CRAB criteria
The CRAB criteria indicate organ damage related to multiple myeloma: Calcium increased > 11 mg/dL, Renal insufficiency (creatinine clearance < 40 mL/min or serum creatinine > 2 mg/dL), Anemia (Hb < 10 g/dL), and Bone lesions.
suggestive features of renal artery stenosis
Treatment-resistant hypertension
Abdominal bruit heard over the flank or epigastrium
Evidence of other atherosclerotic diseases (e.g., CAD, PAD)
suggestive features of amyloidosis
History of a chronic inflammatory condition (e.g., IBD, RA) or chronic infectious disease (e.g., tuberculosis, osteomyelitis)
History of plasma cell dyscrasia
Evidence of other organ involvement (e.g., macroglossia, restrictive cardiomyopathy, hepatosplenomegaly, malabsorption)
nutritional management
fluid intake - avoid dehydration
protein restriction in patients with high CKD category
sodium restriction
pottisum intake adjustment
phosphorous intake adjustment
medication management
for renally cleared drugs - adjust dosing based on patients GFR
avoid nephrotoxics
contrast is highest risk in pateints with GFR < 30
renal replacement therapy
non operative: haemodialysis or peritoneal dialysis
operative: kidney transplatation
dialysis indications
hemodynamic or metabolic complications that are refrectory to medical therapy
eg
volume overload or hypertension
metabolic acidosis
hyperkalaemia
serositis
other symptoms of uremia
refrectory deterioration in nutritional status
ASCVD risk assessment
atherosclerotic cardiovascular disease screening for all patients with CKD
diabetes mellitus screening
screening for hypertension
screening for lipid disorders
cardiovascular risk
blood pressure control
aim for systolic < 120
first line: RAAS inhibitors ie. ACE and ARBs
consider combination therapy with calcium channel blocker or thiazide diuretic
good blood pressure control is crucial to prevent ASCVD complications, reduce mortality and help delay disease progression in patients with CKD
lipid management
fasting lipid panel may show dyslipidaemia (high triglycerides are common)
statin therapy for patients >50 or with comorbidities, or for treatment of ASCVD
antiplatelet therapy
usualy indicated for management of ASCVD
may be considered for primary prevention of ASCVD in high risk individuals
screening for CKD complications
FBC for normochromic, normocytic anaemia
potassium for hyperkalaemia usually seen in advanced CKD
PTH for secondary hyperparathyroidism
hyperphosphataemia and hypocalcaemia typically seen with GFR < 30
Vit D monitoring shows decreased calcidiol and calcitriol
coagulation screen
blood gasses for metabolic acidosis
calcidiol
total body vit D stores
monitoring blood gasses
The kidneys are often no longer able to maintain acid-base balance when the GFR drops below 30 mL/min/1.73 m2. An accumulation of hydrogen ions leads to acidosis.
coagulation screening
normal PT, PTT and platelet count
increased bleeding time due to uraemic platelet dysfunction
common acute complications of CKD
pulmonary oedema
hyperkalaemia
infection
drug toxicity
pulmonary oedema
Due to an inability in patients with very low GFR to clear excess fluids
hyperkalaemia
May be triggered by excessive dietary potassium, nonadherence to diuretic therapy, or a new medication or medication interaction (e.g., ACE inhibitors, potassium-sparing diuretics)
infection as a complication
bacteraemia secondary to UTI or pneumonia
IV catheter-related infection
haemodialysis catheter related infection
peritoneal dialysis-associated peritonitis
calciphylaxis
a rare but potentially life-threatening condition characterized by dermal and subcutaneous arteriolar calcifications that cause painful skin necrosis
riisk factors for calciphylaxis
Most commonly seen in patients with ESRD who are receiving dialysis
Comorbidities: diabetes mellitus, obesity, CKD-mineral and bone disorder, warfarin therapy
clinical features of calciphylaxis
Intensely painful skin lesions, e.g.: livedo reticularis, purpura, plaques, nodules
Necrotic skin ulcerations typically covered with black eschar
Areas of firm, painful, subcutaneous tissue
Secondary bacteremia and sepsis
diagnosis of calciphylaxis
A skin biopsy is required for definitive diagnosis but may provoke new lesions.
Clinical diagnosis may be made in patients with ESRD with a typical presentation.
pathophys of anaemia of chronic kidney disease
decrease in synthesis of erythropoeitn
decrease stimulation of RBC production
normocytic, normochronic anaemia
management of anaemia in CKD
diagnostic studies forr iron deficiency
B12 and folate deficiency
erythropoeitn stimulating agenst
avoid blood transfusions
CKD mineral and bone disorders
abnormalities in mineral and/or bone metabolism in CKD
renal osteodystrophy refers specifically to issues with bone metabolism due to CKD
pathophysiology of CKD mineral and bone disorder
CKD causes hypocalcaemia via two mechanisms
1. decrease in renal excretion of phosphate, hyperphosphataemia, calcium phosphate precipitation
2. decrease in renal hydroxylation of vitamin D, decrease in calcitriol, decrease in intenstinaal Ca bsorption
chronically decrease calcium level can caause secondary hyperparathyroidism, which can progress to tertiary hyperparaathyroidism
clinical features of CKD bone and mineral diseaase
fractures
bone or periarticular pain
muscular weakness and pain
focal vascular calcification (atherosclerotic plaques)
diffuse vascular calcification
treatment of CKD bone and mineral disease
normlise phosphate, calcium and PTH levels
dietary phosphate restriction
phosphate binders
treatment of hyperparathyroidism: supplimentation for vit D, calcimimetics, parathyroidectomy (last line)
secondary hyperprathyroidism
Excessive excretion of parathyroid hormone and hyperplasia of the parathyroid glands in response to low serum calcium levels. Causes include hypovitaminosis D and chronic kidney disease.
