CKD Flashcards
Define CKD
A spectrum of different pathophysiologic process/diseases associated with abnormal kidney function and a progressive decline in GFR
Define Chronic Renal Failure
Irreversible reduction in nephron number, corresponds to CKD stages 3-5
Define ESRD
Accumulation of toxins, fluid and electrolytes normally excreted by the kidney results in the uremic syndrome
Stage 0
GFR >90 with RF for CKD
Stage 1
GFR > 90 with kidney damage/malfunction (persistent proteinuria, abnormal urine sediment, abnormal blood/urine chemistry, abnormal imaging studies
Stage 2
GFR 60-89
Stage 3
GFR 30-59
Symptoms are present
Stage 4
GFR 15-29
Symptoms are present
Stage 5
GFR less than 15
CKD Pathophysiology
1) Mechanisms specific to the etiology (glomerulonephritis, tubulointerstitial disease, kidney development)
2) Progressive reduction of renal mass (hyperfiltration and hypertrophy of remaining nephrons)
Decreased number of nephrons leads to
Hypertrophy and hyperfiltration –> increased pressure and flow –> distortion of glomerular architecture/sclerosis and drop out of remaining nephrons –> destruction of parenchyma
What can cause hypertrophy and hyperfiltrations
Vasoactive hormones
Cytokines
Growth factors
RAS
What can cause distortion of glomerular architecture/sclerosis and drop out of remaining nephrons?
RAS and TGF-beta
What are the consequences of hyperfiltration
Fibrosis and compression of the endothelial cells –> can’t function –> more nephrons are removed –> irreversible process of damage begins
Common risk factors for CKD
HTN and DM Lupus Age Previous AKI Genes
GFR normal
120 mL/min per 1.73 m^2
Lower in women than in men
Mild elevation in SCr
Signifies substantial reduction in GFR
Mild elevation in SCr
Signifies substantial reduction in GFR
Microalbuminuria refers to
the excretion of amounts of albumin too small to detect by regular urinary distick
Monitoring nephron injury
GFR
Albuminuria (24 hr collection)
Protein-to-creatinine ratio
Stage 1 and 2 Symptoms
None related to decreased GFR but may be some related to the renal disease (edema, HTN)
Stage 3 and 4 symptoms
Anemia
Fatigability
Decreasing appetite with progressive malnutrition
Calcium, phosphorus, sodium, potassium, water, acid-base homeostatis and mineral regulating hormone abnormalities
Stage 5 Symptoms
Toxins accumulate –> disturbance in their daily living, well being, nutrional status, water/electrlyte homeostatis
Stage 5 leads to
Uremic syndrome
Leading etiologies of CKD
DM II
Glomerulonephritis
Hypertensive nephropathy
Polycystic kidney disease
Pathophysiology of uremia
Accumulation of toxins that undergo renal excretion
Loss of other renal functions (fluid homeostatis and hormone regulation)
Systemic inflammation and its vascular and nutritional complications (elevated protein C)
Surrogate markers of real toxins are:
Urea and creatinine
Uremia leads to
disturbances in the function of virtually every organ system
Severy complications and consequences of CKD
Cardiovascular
Hematologic (no erythropoietin)
Ca, PO4 and bone (replacement with fibrosis)
Define metabolic acidosis
Abnormally high level of acid and low bicarbonate in blood and other tissues resulting from inability to excrete protons and reabsorb bicarb
Hypervolemia
Na & H2O retention
Extracellular fluid expansion –> HTN and edema
HTN leads to nephron injury acceleration
(no RAAS activation so retention)
Hypovolemia
Na and H2O leads to extrarenal fluid loss +
Impaired renal conservation leads to acute-on-chronic renal failure
Acute on chronic
Inability to concentrate the urine leads to increased water loss and decreased CO
Things that lead to hyperkalemia
Protein catabolism GI hemorrhage ACEi ARBs Transfusion Hemolysis Diuretics
HyperK is seen in
DM
Obstructive and sickle cell nephropathy
Ischemic cardiovascular disease types
Occlusive coronary disease
Cerebrovascular disease
Peripheral vascular disease
Normocytic, normochromic anemia
Insufficient erythropoietin Iron deficiency Impaired iron utilization Severe hyperparathyroidism (bone marrow fibrosis) Shortened RBC survival
Abnormal hemostatis =
Prolong bleeding time
Thromboembolism (nephrotic syndrome - loss of anticoagulants)
Bone manifestations of CKD
High bone turnover with increased PTH levels
Low bone turnover with low or normal PTH
Bone manifestations of CKD
High bone turnover with increased PTH levels
Low bone turnover with low or normal PTH
High bone turnover with increased PTH levels =
Osteitis fibrosa cystica
Low bone turnover with low or normal PTH =
Adynamic bone disease (PTH suppression)
Osteomalacia
Decreased calcium leads to
Bone :Increased bone absorption and Ca efflux
Kidney and intestine: Increased Ca reabs and decreased PO4 reabs
Bone and Kidney due to increased PTH
Intestine due to increased dihyroxycholecalciferol
Too much calcium =
Thyroid gland releases calcitonin which stimulates Ca salt deposit in bone
Too little calcium =
Thyroid gland releases PTH which tells osteoclast to degrade bone matrix to release Ca into blood
Renal osteodystrophy
Increased osteoclastic bone resorption (osteitis fibrosa cystica like disease)
Osteomalacia (decreased matrix mineralization)
Adynamic bone (reduced volume and mineralization
Secondary hyperparathyroidism Patho
Declining GFR leads to reduced PO4 excretion
PO4 stimulates increased PTH and growth of parathyroid gland
Decreased Ca leads to PTH production
Low calcitriol has a direct effect on PTH transcription
Metabolic Acidosis stimulates bone resorption
- GFR
FGR-23 (phosphatonin)
RF for left ventricular hypertrophy and mortality in dialysis pts
Tries to keep normal phosphorus levels
Increases early in CKD and promotes PO4 excretion
CKD has
Hypocalcemia and hyper PO4
CKD has
Hypocalcemia and hyper PO4
Consequences of CKD
Bone pain and fragility Brown tumor Compression syndromes Erythropoietin resistance PTH related muscle weakness and fibrosis of cardiac muscles
