Chronic Kidney Disease + Some random stuff Flashcards
CKD Definition
- Irreversible, progressive damage to parenchyma
- glomerulosclerosis and tubuloinerstitial fibrosis
- decreased GFR
And one of these: - albuminuria
- urine sediment abnormalities
- electrolyte abnormalities,
- histology abnormalities
ESRD
Complete loss of kidney function, requires dialysis or txplant
CKD Stage 1
- GFR >90, evidence of damage w/ no sx +/- proteinuria
CKD Stage 2
- 60-80 GFR
- If caught here, slow progression w/ treatment
CKD Stage 3
30-59 GFR
Often when pt comes to medical attention; most people in this stage (because they start dying after that)
CKD Stage 4
Nephro referral, discuss dialysis vs txplant if
CKD Stage 5
Kidney failure, imminently needs dialysis or txplant
Etiology of CKD
Diabetes > HTN > glomerulonephritis > cystic kidney + vascular dz, tubulointerstitial dz, etc
Pathogenesis of CKD
Primary: diseases which directly damage the kidney
Secondary: non disease events which inflict further damage in all primary kidney diseases; a reduction in renal mass
Dx of CKD
- acute or chronic?
(look at trend of creatinine) - BMP w/ eGFR calculation, urinalysis, microscopic exam, URINE SPOT SAMPLE for proteinuria quantification
- Renal US
Prerenal failure
Almost always renal artery stenosis
Radiology of RF
- fibrosis (echogenic “speckles” kidneys by ultrasound – fibrosis in the renal parenchyma!)
- volume loss in parenchyma (permanenent)
- Enlarged kidneys
- Obstruction
- Cystic dz
Anemia in CKD
- decreased erethropoeitin
- inflammatory cytokines destroy immature RBCs
- hepcidin release –> block iron.
Treat w/ IV iron and give epo analog
Mineral disease in CKD:
Renal mass loss –> decreased GFR–> phosphate retention and decreased vit D –> hypocalcemia and hyperparathyroidism–> renal osteodystrophy
7 Sequelae of CKD
1) Anemia
2) BMD (bone mineral disease)
3) HTN (worsens as GFR decreases)
4) CV disease (leading cause of mortality at all stages of CKD)
5) Uremia –> fatigue, anorexia, nausea, PRURITIS
6) Acidosis, and esp hyperK
7) Volume overload
Treatment of CKD:
- Treat primary dz
- ACEI/ARB +/- diuretic for HTN**
- Tx proteinuria** ACE/ARB
- treat DM
- treat sequelae
- Low K+ diet if hyperK, low P is hypoP, low Na if V overload
- Avoid NSAIDS and contrast (nephrotoxic)
Chronic vs. Acute renal failure
Chronic: time to adapt, finite GFR
Acute: no time to adapt (electrolyte imbalance) often NO GFR.
in CRF the number of functioning nephrons is decreased. whereas in AKI nephrons are globally impaired but not reduced in number.
Pathogenesis of CKD
Common response to kidney damage rather than the result of primary renal disease. (Renal function continues to deteriorate even after primary disease has been treated.)
5 most common primary renal injuries in CKD
Glomerulonephritis diabetes HTN polycystic interstitial nephrites.
5 secondary phenomena in CKD
Glomerular hypertrophy (increase in SNGFR) Intraglomerular HTN Phosphate retention and hyperparathyroid Systemic HTN Hyperlipidemia
5 kidney problems that NSAIDs cause
1) Papillary necrosis (RBC in urine, pain, similar sx to kidney stone)
2) ATN
3) HTN (via inhibition of prostaglandins)
4) MCD + AIN
5) Pre-renal AZ (hemodynamic effect)
Maintenance of acid/base balance during CKD?
Increased ammonia-genesis in the remaining working nephrons.
Three factors which control K+ secretion
- Renal Flow Rate
- Aldosterone secretion (^ aldo causes excretion of K. Remember that hyperkalemia stimulates aldo)
- acid/base status (acidosis favors K+ retention)
Type I RTA
Distal RTA is caused by defects in distal hydrogen ion excretion
Type II RTA
Proximal RTA is caused by defects that reduce the capacity to reclaim filtered bicarbonate in the proximal tubule
Type IV RTA
Hyperkalemic RTAs include hypoaldosteronism (type 4) and a disorder called voltage-dependent RTA
Renin Release stimulated by?
1) Macula densa senses low NaCl in tubule and signals to JGA to release renin (to increase GFR)
2) SNS stimulates renin release
In the kidney, the macula densa is an area of closely packed specialized cells lining the wall of the cortical thick ascending limb, at the transition to the distal convoluted tubule.
The cells of the macula densa are sensitive to the concentration of sodium chloride in the late thick ascending limb. A decrease in sodium chloride concentration initiates a signal from the macula densa that has two effects: (1) it decreases resistance to blood flow in the afferent arterioles via vasodilation, which increases glomerular capillary hydrostatic pressure and helps return glomerulus filtration rate (GFR) toward normal, and (2) it increases renin release from the juxtaglomerular cells of the afferent and efferent arterioles, which are the major storage sites for renin
Treatment for hyperparathyroidism 2/2 renal disease
phosphate binders, then vitamin D
Vitamin D synth
Step 1) Skin
Step 2) Liver
Step 3) Kidney (need this last step for functioning Vit D)
Vitamin D actions
1) Acts on intestine to stimulate calcium and phosphate absorption
2) stimulates phosphate reabsorption in the kidney and increases bone turnover
Three contributors to MBD
1) hyperPTH
2) vitamin D deficiency
3) chronic metabolic acidosis
