Nephrology Flashcards by Jc Reyes

Site of erythropoietin (EPO) production

Interstitial cells of the peritubular capillaries

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Active form of Vitamin D

1,25-dihydroxycholecalciferol (calcitriol)

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Contains vasa recta and has longer loops of Henle

Juxtamedullary nephrons (less common than cortical nephrons)

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Components of the juxtaglomerular apparatus

Macula densa (walls of the dital tubule; detects changes in BP)

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Physiologic function of renin

None (merely converts angiotensinogen from the liver to angiotensin I)

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Physiologic function of angiotensin I

None (merely converted to angiotensin II due to ACE in the lungs)

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Physiologic functions of angiotensin II

Vasoconstricts afferent and efferent arteriole (efferent > afferent)

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Site of aldosterone production

Zona glomerulosa of the adrenal cortex

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Aldosterone actions

Increases Na+ reabsorption, K+ secretion, H+ secretion

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ADH actions

Insertion of aquaporins (AQP-2) in the collecting ducts

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Triggers for ADH secretion

Increased plasma osmolarity

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Increases GFR

Afferent arteriolar vasodilation

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Decreases GFR

Afferent arteriolar vasoconstriction

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Principal cells

Absorb Na+ and H20 and secrete K+

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Intercalated cells

Absorb K+ and secrete H+

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Tubuloglomerular feedback

Macula densa feedback

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Glomerulotubular balanca

“Percentage of solute reabsorbed is held constant”

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Substances with no transport maximum and renal threshold

Sodium and all passively transported solutes

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Ascending limb of the Loop of Henle is permeable to

Solutes (Mnemonic: asin-ding limb is permeable to solutes)

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Descending limb of the Loop of Henle is permeable to

Water

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Normal pH in various fluid sites

Arterial blood: 7.4

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Acid-base abnormalities caused by diuretics

Metabolic acidosis: acetazolamide (Mnemonic: acid-azolamide)

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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

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Bricker’s Trade-Off Hypothesis

Some physiologic adaptations to nephron loss also produce unintended clinical consequences

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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

1. 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

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