Nephrology Flashcards
Site of erythropoietin (EPO) production
Interstitial cells of the peritubular capillaries
Active form of Vitamin D
1,25-dihydroxycholecalciferol (calcitriol)
Contains vasa recta and has longer loops of Henle
Juxtamedullary nephrons (less common than cortical nephrons)
Components of the juxtaglomerular apparatus
Macula densa (walls of the dital tubule; detects changes in BP)
Physiologic function of renin
None (merely converts angiotensinogen from the liver to angiotensin I)
Physiologic function of angiotensin I
None (merely converted to angiotensin II due to ACE in the lungs)
Physiologic functions of angiotensin II
Vasoconstricts afferent and efferent arteriole (efferent > afferent)
Site of aldosterone production
Zona glomerulosa of the adrenal cortex
Aldosterone actions
Increases Na+ reabsorption, K+ secretion, H+ secretion
ADH actions
Insertion of aquaporins (AQP-2) in the collecting ducts
Triggers for ADH secretion
Increased plasma osmolarity
Increases GFR
Afferent arteriolar vasodilation
Decreases GFR
Afferent arteriolar vasoconstriction
Principal cells
Absorb Na+ and H20 and secrete K+
Intercalated cells
Absorb K+ and secrete H+
Tubuloglomerular feedback
Macula densa feedback
Glomerulotubular balanca
“Percentage of solute reabsorbed is held constant”
Substances with no transport maximum and renal threshold
Sodium and all passively transported solutes
Ascending limb of the Loop of Henle is permeable to
Solutes (Mnemonic: asin-ding limb is permeable to solutes)
Descending limb of the Loop of Henle is permeable to
Water
Normal pH in various fluid sites
Arterial blood: 7.4
Acid-base abnormalities caused by diuretics
Metabolic acidosis: acetazolamide (Mnemonic: acid-azolamide)
Intact Nephron Hypothesis by Neil Bricker
Decreases in the number of functioning nephrons causes remaining nephrons to carry a larger burden of transport, synthetic function and regulatory function
Bricker’s Trade-Off Hypothesis
Some physiologic adaptations to nephron loss also produce unintended clinical consequences
Hyperfiltration Hypothesis by Barry Brenner
Some adaptations accelerate the deterioration of residual nephrons
Standard test for measurement of albuminuria
Accurate 24-hour urine collection
Most useful renal imaging study
Renal ultrasound
The only test to establish etiology in early-stage CKD in the absence of a clinical diagnosis
Renal biopsy
Most sensitive test for renal vein thrombosis (RVT)
CT angiography
Imaging test for diagnosis of nephrolithiasis
Helical computed tomography (CT) scanning without radiocontrast enhancement
Most common form of renal replacement therapy for AKI
Hemodialysis
Clear indications for initiation of renal replacement therapy in patients with CKD
- Uremic pericarditis
Best potential for complete renal rehabilitation
Kidney transplantation
Educational programs should be commenced
No later than stage 4 CKD
Most common therapeutic modality for end-stage renal disease (ESRD)
Hemodialysis
Leading cause of ESRD
Diabetes mellitus
Dialysis access with highest long-term patency rate
Fistula
Most important complication of arteriovenous grafts
Thrombosis of the graft and graft failure
Most common acute complication of hemodialysis, particularly among DM patients
Hypotension
Preferred buffer in peritoneal dialysis solutions
Lactate
Most common additives to peritoneal dialysis solutions
Heparin
Most common organisms in peritoneal dialysis-related peritonitis
Gram-positive cocci including Staphylococcus (reflecting the origin from the skin)
Absolute indication for the urgent initiation of or intensification of dialysis prescription
Uremic pericarditis
Definition of AKI (Acute Kidney Injury)
A rise of at least 0.3 mg/dL within 48h or 50% higher than baseline within 1 week; or reduction in urine output to <0.5 mL/kg/h for >6 hours
Definition of oliguria
<400 mL/24h
Associated with multiple myeloma
Renal amyloidosis
Most common cause of Acute Renal Failure (ARF)
Acute Tubular Necrosis (ATN)
Most common form of AKI
Prerenal Azotemia (from Harrison’s IM)
Patchy necrosis, PCT & LH affected, relatively short lengths of tubules affected
Ischemic-type ATN (e.g. in hypovolemia)
Extensive necrosis, PCT and DT affected, relatively longer lengths of tubules
Toxic-type ATN (e.g. in use of aminoglycosides, radiocontrast dyes)
Three broad categories of AKI
Prerenal Azotemia
Most common clinical conditions associated with prerenal azotemia
Hypovolemia
Most common causes of intrinsic AKI
Sepsis, ischemia, and nephrotoxins
Most common clinical course of contrast nephropathy
A rise in SCr beginning 24-48 hours following exposure
Most common protein in urine and produced in the thick ascending limb of the loop of Henle
Uromodulin/ Tamm-Horsfall Protein
Hallmark of AKI
Buildup of nitrogenous waste products, manifested as an elevated BUN concentration
Causes of large kidneys observed in CKD
Diabetic nephropathy
Can provide definitive diagnostic and prognostic information about CKD
Kidney biopsy
Definitive treatment of the hepatorenal syndrome
Liver transplantation
Cerebral edema
Severe hemodynamic instability
Continuous Renal Replacement Therapy is often preferred in patients with
Significant volume overload
Chronic renal failure typically corresponds to
Stage 3-5 CKD
ESRD refers to
Stage 5 CKD (<15% GFR)
Screening test for early detection of renal disease
Microalbuminuria (especially in DM)
Major side effect of calcium-based phosphate binders
Total-body calcium accumulation and hypercalcemia
Leading cause of morbidity and mortality in patients at every stage of CKD
Cardiovascular disease (CVD)
Major risk factor for ischemic CVD
Presence of any stage of CKD
Among the strongest risk factors for cardiovascular morbidity and mortality in CKD
Left ventricular hypertrophy and dilated cardiomyopathy
Absence of hypertension in CKD may signify
Salt-wasting form of renal disease
Stage of CKD where normocytic, normochromic anemia appears
As early as Stage 3 CKD
Primary cause of anemia
Insufficient production of EPO by the diseased kidneys
Target hemoglobin concentration in CKD
100-115 g/L
Stage of CKD where peripheral neuropathy usually becomes clinically evident
Stage 4 CKD
Stage of CKD where assessment for protein-energy malnutrition should begin
Stage 3 CKD
Indication for therapy with ACE inhibitors for ARBs
Protein excretion >300 mg
Derives from the breakdown of urea to ammonia in saliva and is often associated with an unpleasant metallic taste (dysgeusia)
Uremic fetor
Most important initial diagnostic step in the evaluation of a patient presenting with elevated serum creatinine
To distinguish newly diagnosed CKD from acute or subacute renal failure
Classic lesion of secondary hyperparathyroidism; high bone turnover with increased PTH levels
Osteitis fibrosa cystica
Low bone turnover with low or normal PTH levels
Adynamic bone disease and Osteomalacia
Devastating condition seen almost exclusively in patients with advanced CKD
Calciphylaxis (Calcific uremic arteriolopathy)
Seen in patients with CKD who have been exposed to gadolinium
Nephrogenic fibrosing dermopathy
“Thyroidization” (appearance similar to thyroid follicles) of the kidney
Chronic glomerulonephritis (GN)
RBC casts or dysmorphic RBCs seen in the sediment
GN
Most common causes of glomerulonephritis throughout the world (save for subacute bacterial endocarditis in the Western hemisphere)
Malaria and schistosomiasis (closely followed by: HIV, chronic hepatitis B and C)
Prototypical for acute endocapillary proliferative GN
Poststreptococcal GN (PSGN)
Streptococcal strains associated with impetigo
M types 47, 49, 55, 2, 60, and 57
Streptococcal strains associated with pharyngitis
M types 1, 2, 4, 3, 25, 49, and 12
Kidneys have subcapsular hemorrhages with a “flea-bitten” appearance
Endocarditis-associated GN
Primary treatment for endocarditis-associated GN
Eradication of the infection with 4-6 weeks of antibiotics
May produce nephrotic or nephritic signs and symptoms
Membranoproliferative GN (MPGN)
Type I MPGN characteristics
Presence of subendothelial deposits; low C3
Type II MPGN characteristics
Intramembranous deposits, ribbon-like pattern, IgG autoantibody; low C3
Most proliferative of the three types of MPGN
Type I MPGN
Pathologic changes of FSGS are most prominent in
Glomeruli located at the corticomedullary junction (if the renal biopsy specimen is from superficial tissue, the lesions can be missed, leading to a misdiagnosis of MCD)
Has the highest reported incidences of renal vein thrombosis, pulmonary embolism, and deep vein thrombosis
Membranous Nephropathy (MGN)
Sensitive indicator for the presence of diabetes but correlates poorly with the presence or absence of clinically significant nephropathy
Thickening of the GBM
Earliest manifestation in ~40% of patients with diabetes who develop diabetic nephropathy
Increase in albuminuria detected by sensitive radioimmunoassay
Potent risk factor for cardiovascular events and death in patients with type 2 diabetes
Microalbuminuria
Most renal amyloidosis is the result of
Fibrillar deposits of immunoglobulin light chains
Lesion in HIV-associated nephropathy
FSGS
