Renal

Question 1

What is azotemia?

Answer 1

An elevation of blood urea nitrogen and creatinine levels and usually reflects a decreased glomerular filtration rate. When azotemia gives rise to clinical manifestations and systemic biochemical abnormalities, it is termed uremia.

Question 2

What is the difference between prerenal and postrenal azotemia?

Answer 2

Prerenal: encountered when there is hypoperfusion of the kidneys (usually due to reduced extracellular fluid volume) This decreases GFR in absence of renal parecnchymal damage and is usually reversible if the hypoperfusion is corrected in time.
Postrenal: When urine outflow is obstructed. Relief of the obstruction is followed by correction of the azotemia.

Question 3

What are characteristics of nephrotic syndrome?

Answer 3

Proteinuria: 3.5 g or more.
Hypoalbuminemia: plasma albumin levels less than 3g/dL.
Generalized edema.
Hyperlipidemia.
Derangement in capillary walls of glomeruli that results in increased permeability to plasma proteins.

Question 4

What are characteristics of nephritic syndrome?

Answer 4

Hematuria.
Proteinuria: subnephrotic range.
Azotemia: nitrogenous waste products in blood.
Hypertension.
Acute onset.
Inflammatory lesions of glomeruli.

Question 5

What is nephrin?

Answer 5

Transmembrane glycoprotein making up majority of filtration slits, rare mutation of nephrin results in proteinuria.

Question 6

What diseases are associated with primary glomerular disease?

Answer 6

1. Minimal-change disease
2. Focal segmental glomerulosclerosis.
3. Membranous nephropathy.
4. Acute postinfectious glomerulonephritis.
5. IgA nephropathy.
6. Dense deposit disease.
7. C3 glomerulonephritis

Question 7

What diseases are associated with secondary glomerular disease?

Answer 7

1. Lupus nephritis (systemic lupus erythematous)
2. Diabetic nephropathy.
3. Amyloidosis
4. Glomerulopathy secondary to multiple myeloma.
5. Goodpasture syndrome.
6. Microscopic polyangiitis.
7. Granulmatosis with polyangiitis.
8. Henoch-schonlein purpura.
9. Bacterial endocarditis
10. Thrombotic microangiopathy

Question 8

What are mechanisms of antibody deposition?

Answer 8

1. Deposition of circulating antigen-antibody complexes in the glomerular capillary wall or mesangium.
2. Antibodies reacting in situ within the glomerulus either with fixed (intrinsic) glomerular antigens or with extrinsic molecules that are planted in the glomerulus.

Question 9

Clinical presentation and pathogenesis of Minimal change disease?

Answer 9

Presentation: nephrotic syndrome. More prevalent in children.
Pathogenesis: unknown. Manifested by proteinuria and effacement of  glomerular foot  processes without  antibody deposits.

Question 10

Clinical presentation and pathogenesis of focal segmental glomerulosclerosis?

Answer 10

Presentation: Nephrotic syndrome (nonnephrotic range proteinuria). More prevalent in adults.
Pathogenesis: Unknown. Glomeruli show focal and segmental obliteration of capillary lumina and loss of foot processes.

Question 11

Clinical presentation and pathogenesis of membranous nephropathy?

Answer 11

Presentation: nephrotic syndrome. More prevalent in adults.
Pathogenesis: Caused by autoimmune response, most often directed against podocytes. Characterized by granular subepithelial deposits of antibodies with glomerularbasal membrane “spike” formation, thickening and loss of podocyte foot processes, but little or no inflammation.

Question 12

Clinical presentation and pathogenesis of acute post infectious glomerulonephritis?

Answer 12

Presentation: nephritic syndrome.
Pathogenesis: typically occurs after streptococcal infection in children and young adults but may occur  following infection with many other  organisms. It is caused by deposition of immune complexes, mainly in the subepithelial spaces, with abundant neutrophils and proliferation of glomerular cells.

Question 13

Clinical presentation and pathogenesis of IgA nephropathy?

Answer 13

Presentation: Nephritic syndrome. Typically presents in childhood.
Pathogenesis: Abnormal IgA not recognized as self, IgG attacks and forms immune complex. Characterized by mesangial deposits of IgA containing immune complexes. Most common form of glomerulonephritis worldwide. May lead to renal failure.

Question 14

Clinical presentation and pathogenesis of goodpasture syndrome (Anti-GBM disease)?

Answer 14

Presentation: Nephritic syndrome. A.K.A. rapidly progressive glomerulonephritis. (RPGN)
Pathogenesis: Autoantibodies against collagen alpha 3 chain that cause inflammation response and damage glomerular basement membrane.

Question 15

What is amyloidosis?

Answer 15

Condition associated with several disorders. Amyloid (fibrillar protein) buils up in heart, kidney, liver, etc= tissue damage/functional compromise

Question 16

Define acute post-infectious glomerulonephritis.

Answer 16

Acute nephritic syndrome in which inflammation of the glomerulus is manifested by proliferation of cellular elements secondary to an immunologic mechanism. Injury caused by complement activation by classical pathway. Characterized by edema, hematuria, proteinuria, hypertension.

Question 17

Common etiologic agents of acute post infectious glomerulonephritis?

Answer 17

1. Group A streptococcus
2. Pneumococcal and staphylococcal organisms.
3. Viral diseases: mumps, measles, varicella, Hep B and C

Question 18

What are common etiologic agents, pathogenesis, and clinical presentation of drug-induced interstitial nephritis?

Answer 18

Etiologic agents: penicillins, antibiotics, diuretics, proton-pump inhibitor, NSAIDs.
Pathogenesis: Immune reaction to a drug (IgE or T-cell). Tubulointerstitial inflammation and edema.
Clinical presentation: fever, eosinophilia, rash, renal abnormalities

Question 19

What is Acute tubular injury?

Answer 19

Damage to tubular epithelial cells and an acute decline in renal function. Common findings include elecrtrolyte abnormalities, azotemia, oliguria and decreased GFR.

Question 20

What are underlying causes of acute tubular injury?

Answer 20

1. Ischemic: period of inadequate blood flow to kidney (trauma, pancreatitis, septicemia)
2. Nephrotoxic: caused by variety of poisons, including heavy metals (mercury), organic solvents, some drugs/antibiotics, radiographic contrast agents.

Question 21

What is nephrosclerosis?

Answer 21

Sclerosis of small renal arteries and arterioles that is strongly associated with hypertension.

Question 22

Describe arterial lesions associated with nephrosclerosis.

Answer 22

Fibrous medial and intimal thickening (fibroelastic hyperplasia). Hyalinization of arteriolar walls (hyaline arteriosclerosis). Lesions that increase in frequency and severity with age, HTN, diabetes. Loss of concentrating ability and diminished GFR, mild proteinuria. African americans are susceptible population.

Question 23

Describe renal changes of malignant hypertension.

Answer 23

1. Thrombotic microangiopathy.
2. Fibrinoid necrosis of arterioles.
3. Platelets cause intimal hyperplasia of vessels (hyperplastic arteriosclerosis) causing narrowing that leads to kidney ischemia.

Question 24

What is pathogenesis of Chronic kidney disease?

Answer 24

Scarring of nephrons. Sclerosed glomeruli, tubules, interstitium, vessels.
Adaptive mechanisms: hyperfiltration, increase excretion rate solutes per nephron, decreased reabsorption, increased secretion.

Question 25

What are morphological changes in CKD?

Answer 25

1. kidneys are symmetrically contracted.
2. Red-brown, diffusely granular.
3. Obliteration of glomeruli.
4. Interstitial fibrosis.
5. Difficult to ascertain if primary lesion was glomerular, vascular, tubular, interstitial.

Question 26

What is clinical course of CKD?

Answer 26

1. May develop insidiously and be discovered late in its course.
2. Glomeruli undergo sclerotic changes and result in nephron loss.
3. Some degree of proteinuria.
4. Hypertension
5. Microscopic hematuria.
6. Prognosis poor without treatment.
7. Dialysis, transplantation, or death.