Renal Pathology Flashcards

Question

What is the hallmark of FSGN on histology?

Answer 1

epithelial damage Light micro: focal and segmented lesions; mesangial collapse and sclerosis Electron micro: Degeneration and focal disruption of epithelial cells with diffuse effacement of foot processes, (podocytes) Immunofluorescence: IgM and C3 in the sclerotic areas and the mesangium

Answer 2

Spontaneous remission is rare Children have a better prognosis with Minimal Change Disease Poor response to corticosteroids therapy in FSGN Whereas minimal change disease (MCD) shows normal histology, FSGS is associated with sclerosis under the microscope with proteinuria. Progression to chronic kidney dz, with 50% developing ESRD within ten years

Answer 3

Common worldwide (most common glomerulonephritis) Mesangial IgA immune deposits Glomerulonephritis of varying severity Idiopathic or after an upper respiratory tract infections or gastroenteritis; gross hematuria Hematuria lasts a few days, subsides, and returns every few months Maintain normal kidney function for decades 15-40% will develop chronic renal failure over a period of 20 years Occurs with increased frequency in individuals with gluten enteropathy and liver disease 5-10% develop acute nephritic syndrome with some developing rapidly progressive glomerulonephritis

Answer 4

Defective type IV collagen- glomerular basement membrane X linked autosomal dominant/autosomal recessive forms exist Nerve deafness, lens dislocation, posterior cataracts and corneal dystrophy Manifested by hematuria and progression to chronic renal failure Males Variability age of onset EM: Irregular thickening and thinning of the GBM with splitting and lamination of the lamina densa Buzzword: "Basketweave appearance"

Answer 5

Leading cause of CKD ESRD occurs in up to 40% of diabetics Histopath changes are similar for type I and type II diabetics Three lesions are encountered: Glomerular Renal vascular (arteriolosclerosis) Pyelonephritis Diabetic microangiopathy- glomerular lesions and thickening of basement membranes Pyelonephritis (kidney infection spreading from UTI)

Answer 6

SLE- 50 % renal involvement (predominant effects females) Diabetes- arteriolosclerosis- microangiopathy- pyelonephritis Sickle cell disease

Answer 7

Renal disease in > 50% of patients Clinical Presentation: Persistent proteinuria Nephritic synd; Nephrotic synd; Rapidly Progressing Glomerular Nephritis; Membranous; Acute and chronic renal failure Pathogenesis: Immune complex deposition; Anti-dsDNA antibodies deposited within the mesangium and non-uniformly along the basement membrane In situ and immune complex deposition Wide variability in injury patterns Six different classes of systemic lupus classified pathologically

Answer 8

Glomerular lesions: Capillary BM thickening Diffuse mesangial sclerosis Nodular glomerulosclerosis Tubular lesions: BM thickening Microangiopathy: - Hyaline sclerosis of the afferent and efferent arterioles

Answer 9

Hemoglobinopathy Hereditary- mutation lead to structural abnormalities Sickling of blood cells Widespread microvascular obstruction-ischemic damage and pain Variable prognosis Hematuria, proteinuria and diminished concentrating ability (nephritic syndrome) Nephrotic syndrome can also occur

Answer 10

Papillary ischemia and necrosis Injury due to accelerated sickling of RBC’s in the medullary vasa recta because of low oxygen tension

Answer 11

Refers to a rapid decline in the glomerular filtration rate and is concurrent with dysregulation of fluid and electrolyte balance Caused by injury to the glomerular, intersitial, vascular, or tubular areas leading to Ischemia- interruption of blood flow- massive hemorrhage, severe burns, dehydration, prolonged diarrhea, CHF Direct toxic injury- endogenous (hemoglobin- monoclonal light chains) exogenous- drugs, radiocontrast dyes, heavy metals and organic solvents Reduced urine production Pulmonary edema Hypotension (ATN) or hypertension ( Intravascular volume expansion) Peripheral edema- impaired renal salt excretion Retention of metabolic waste products May result in oliguria or anuria

Answer 12

Assoc with nonsteroidal anti-inflam drugs (NSAID’s) Aspirin, celebrex, ibuprofen (advil, motrin), naproxen (aleve)… NSAID’s are cyclooxygenase inhibitors Adverse renal effects are related to their ability to inhibit cyclooxygenase-dependent prostaglandin synthesis The selective COX-2 inhibitors affect the kidney because COX-2 is expressed in kidneys

Answer 13

Sudden-onset kidney failure OTC painkillers: Aspirin, ibuprofen and naproxen Fluid loss or decreased fluid intake Wide range: single dose-short term use of not more than 10 days Risk factors: SLE, advanced age, heavy alcohol consumption Emergency dialysis- Kidney damage is usually reversible

Answer 14

lead, mercury, arsenic, and cadmium

Answer 15

Acute kidney injury (Decreased synthesis of vasodilatory prostaglandins causing ischemia) Acute hypersensitivity interstitial nephritis Acute interstitial nephritis and minimal change disease (nephrotic syndrome) Injury to podocytes mediated by cytokines released as part of the inflammatory process ``` Membranous nephropathy (nephrotic syndrome) Unclear pathogenesis ```

Answer 16

Nondominant arm Advantages: Lower infection rates Higher blood flow rates Lower thrombosis/stenosis rates Disadvantages: Longer maturation time Aneurysm formation

Answer 17

Artificial vessel (graft) made of synthetic material Forearm Upper arm Lower extremity Advantages: Can be use sooner Disadvantages Pseudoaneurysm formation Higher infection rates Blood clots

Answer 18

Occurs in 2% to 9% of patients receiving hemodialysis Staphylococcal infections that develop at the site of the graft/fistula/catheter Viridans and lactobacillus Antibiotic prophylaxis before invasive dental procedures is NOT supported by the AHA , need consultation with MD Comorbidities

Answer 19

Routine Urinalysis Color, turbidity, pH, specific gravity, protein, glucose, ketones; Microscopic analysis Routine Blood Tests Na, K, Cl, glucose, BUN, creatinine

Answer 20

Biochemical abnormality that refers to an elevation of blood urea nitrogen and creatinine levels Usually related to a decreased glomerular filtration rate Types of Azotemia include: Prerenal azotemia Hypoperfusion of the kidneys Postrenal azotemia Urine flow obstruction distal to the kidney Intrinsic renal disease

Answer 21

When azotemia becomes associated with a constellation of clinical signs and symptoms and biochemical abnormalities, it is termed uremia Uremia is notable for a number of extrarenal manifestations Uremic gastroenteritis, peripheral neuropathy, uremic fibrinous pericarditis, etc.

Answer 22

Glomerular disease Dominated by an acute onset of hematuria, RBC casts in the urine, diminished GFR, mild to moderate proteinuria, and hypertension KEEP IS THE HEMATURIA

Answer 23

Glomerular disease Dominated by HEAVY proteinuria (3.5 gm/ day) which leads to a significant loss of serum albumin (hypoalbuminemia,), which leads to low oncotic pressure (edema), which leads to sodium and water retention as well as hyperlipidemia, and lipiduria

Answer 24

Highly cationic antigens tend to cross the basement membrane (subepithelial location) Highly anionic antigens are excluded (subendothelial location) Neutral charge complexes tend to localize to the mesangium Large complexes tend to be excluded from filtration

Answer 25

Hypercellularity - Proliferation of mesangial cells or endothelial cells - Infiltration of leukocytes - Formation of crescents ``` Basement membrane thickening -Deposition of material (proteoglycans or more type IV collagen) -Increased synthesis of proteins -Formation of additional GBM layers ``` Hyalinosis - Accumulation of eosinophilic proteinaceous material which obliterates the capillary lumens Sclerosis -Deposition of extracellular collagenous material

Answer 26

Primary Glomerulonephropathies – refer to disorders in which the kidney is the predominant organ involved ``` Secondary glomerular diseases -- Systemic diseases in which the kidneys are affected > Systemic lupus erythematosus >Hypertension >Diabetes mellitus >Alport syndrome ```

Answer 27

``` Postinfectious glomerulonephritis Goodpasture syndrome Chronic glomerulonephritis Membranous nephropathy Minimal change disease Focal segmental glomerulosclerosis Membranoproliferative glomerulonephritis (MPGN Type I) Dense deposit disease (MPGN Type II) IgA nephropathy ```

Answer 28

Anti-GBM antibody > Type I, Goodpasture syndrome ``` Immune complex > Lupus nephritis >Henoch-Schonlein purpura >IgA nephropathy > Postinfectious glomerulonephritis ``` Pauci-immune > ANCA-associated >Granulomatosis with polyangiitis >Microscopic polyangiitis

Answer 29

Arteriolosclerosis Diabetic microangiopathy - Glomerular lesions - Thickening of basement membranes Pyelonephritis

Answer 30

Ischemic or toxic tubular injury - Acute tubular necrosis Inflammatory reactions of the tubules and interstitium - Tubulointerstitial nephritis

Answer 31

is a reversal lesion that occurs in a variety of clinical settings Most of the clinical scenarios have a period of inadequate blood flow to the peripheral organs Ischemic acute tubular necrosis May be associated with hemolytic crises Mismatched blood transfusions (hemoglobinuria) Skeletal muscle injury (myoglobinuria) Characterized by destruction of tubular epithelial cells (pathologic) Acute suppression of renal function (clinical) Most common cause of acute renal failure

Answer 32

``` Organic vascular obstruction -Diffuse involvement of intrarenal vessels from systemic disease (hypertension) ``` Severe glomerular disease -Rapidly progressive glomerulonephritis Acute tubulointerstitial nephritis - Hypersensitivity to drugs Massive infection - Pyelonephritis Disseminated intravascular coagulation Urinary obstruction - Tumors, prostatic hyperplasia Acute tubular necrosis

Answer 33

Gentamicin and other penicillin antibiotics Contrast agents (for CTs and MRIs) Poisons (mercury) Organic solvents (carbon tetrachloride) Pathogenesis: Two critical events - Tubular injury Persistent and severe disturbances in blood flow So if theres injury to the tubules itself, dysfunction with sodium transport, the kidneys will recognize that dysfunction, further constrict blood vessels and lead to a persistent and severe disturbance to blood flow. Sort of a feedback mechanism that makes things worse without clinical attention.

Answer 34

Reversible structural changes: - Cellular swelling - Loss of brush border - Blebbing - Loss of polarity - Cell detachment Irreversible structural changes: - Necrosis - Apoptosis ``` Functional damage: - Depletion of ATP - Accumulation of intracellular calcium - Activation of proteases and phospholipases - Generation of reactive oxygen species ```

Answer 35

Recruitment of leukocytes Luminal obstruction by injured tubular cells Interstitial edema leading to tubule collapse Tubuloglomerular feedback

Answer 36

Ischemic: Most vulnerable locations are the straight portion of the proximal tubule and the ascending thick limb in the renal medulla Toxic: Injury occurs in the proximal convoluted tubules Hyaline casts are common, particularly in the distal tubules and collective ducts Interstitial edema and Accumulation of leukocytes in both

Answer 37

Highly variable 1. Initiating - Lasts about 36 hours - Dominated by the inciting event - Slight decline in urine output and a rise in BUN 2. Maintenance - Sustained decreases in urine output - Salt and water overload - Rising BUN - Hyperkalemia - Metabolic acidosis - Uremia 3. Recovery stages - Steady increase in urine volume (up to 3/L a day) - Tubules are still damaged, so large amounts of water, sodium, and potassium are lost in the urine - Hypokalemia becomes a problem - Increased risk of infection Prompt and appropriate treatment is the difference between life and death

Answer 38

Can be acute or chronic Distinguished from glomerular diseases by defects in tubular function (impaired ability to concentrate urine, salt wasting, metabolic acidosis) and a lack of glomerular hallmarks (nephritic or nephrotic syndrome)

Answer 39

``` Infections Toxins Metabolic Diseases Physical Factors Neoplasms Immunologic Reactions Vascular Diseases Others ```

Answer 40

One of the most common diseases of the kidney Defined by inflammation affecting the tubules, interstitium, and renal pelvis Acute pyelonephritis = Bacterial infection and is associated with UTI Chronic pyelonephritis = More complex pathogenesis Two routes of infection: - Hematogenous infection (a systemic infection – if you have a pneumonia, infective endocarditis, some other localized infection or systemic infection within the body) - Ascending infection (coming from a UTI)

Answer 41

Suppurative inflammation of the kidney Patchy, interstitial inflammation Intratubular aggregates of neutrophils Tubular necrosis Glomeruli are relatively resistant - Extensive infections with involve all compartments Discrete, focal lesions Wedge shaped areas can develop frank papillary necrosis, so complete destruction & necrosis of the renal papilla. If the infection continues to accumulate & pus gathers in the area of the calyces in the kidney, that is what is called pyonephrosis – so pus in the kidney. & then there can be direct extension into the perinephric soft tissues & you can develop peripnephric abscess which can be in the acute phase or the chronic phase.

Answer 42

Mainly seen in diabetics, sickle cell disease, and urinary tract obstruction Usually bilateral Grossly, see necrosis of the tips of the papilla Microscopically, see coagulative necrosis

Answer 43

Seen when there is total or near total obstruction Pus fills up the pelvis, calyces, and ureter Extension of the inflammation into the surrounding tissues Healing occurs Neutrophils are replaced by macrophages, lymphocytes, and plasma cells Scars form >Tubular atrophy, interstitial fibrosis, and lymphocytes > Patchy, jigsaw pattern > Fibrous depressions on the surface

Answer 44

Chronic tubulointerstitial inflammation and scarring involve the calyces and pelvis Reflux nephropathy Chronic obstructive pyelonephritis

Answer 45

More common form Occurs early in childhood as the result of UTI and congenital vesicoureteral reflux May be unilateral or bilateral, leading to renal insufficiency

Answer 46

Recurrent infections superimposed on localized or diffuse obstructive lesions Unilateral in the case of calculi Bilateral in the case of congenital lesions Repeated bouts of inflammation and scarring

Answer 47

Second most common cause of acute kidney injury (after pyelonephritis) Injury occurs in at least three ways 1. Triggers an interstitial immunologic reaction (hypersensitivity nephritis) 2. Causes acute tubular injury 3. Causes subclinical but cumulative damage to tubules

Answer 48

``` Can occur with a variety of drugs: Synthetic penicillins Rifampin Diuretics NSAIDs Allopurinol Others ``` Fever, esoinophilia, rash (25% of patients), and renal abnormalities 15 days after drug exposure (range of 2-40) Hematuria Mild proteinuria Leukocyturia (eosinophils) ``` Clinical evidence suggests a hypersensitivity reaction (Type I) Latent period Eosinophilia and rash Not dose related Recurrence after re-exposure IgE elevations (in some patients) ``` Other cases suggest a T-cell mediated process with granulomatous inflammation and a positive skin test (Type IV)

Answer 49

Bence-Jones proteinuria and cast nephropathy: BJ proteins are directly toxic to the tubules BJ proteins can combine with Tamm-Horsfall proteins and obstruct tubular lumens Amyloidosis Free light chains occur in 6-24% of MM patients Light chain deposition disease: May deposit in the GBM and mesangium Hypercalcemia and hyperuricemia

Answer 50

Describes sclerosis of renal arterioles Strongly associated with hypertension Cause and consequence of nephrosclerosis Medial and intimal thickening of the vessels as a response to a variety of factors Hyalinization of the arteriolar walls Patchy ischemic atrophy Tubular atrophy and interstitial fibrosis Glomerular changes

Answer 51

Narrowing at the origin of the renal artery by atheromatous plaque (70%) Fibromuscular dysplasia is the second most common cause Abnormal fibrous thickening of the intima, media, or adventitia Renal artery narrowing stimulates renin secretion leading to production of the vasoconstrictor angiotensin II

Answer 52

So as the kidney is backing up things start to dilate. You get progressive atrophy of the kidney. Might be slightly to massively enlarged over time. The important thing is it’s going to decrease it’s functional capacity and people affected will develop chronic kidney disease over time.

Answer 53

Most common pediatric renal tumor Peak incidence is 2 to 5 years 95% occur before 10 years of age Approximately 5-10% involve both kidneys Clinical Features: Abdominal mass Hematuria Intestinal obstruction Hypertension Cure rate is approximately 90%

Answer 54

Most common adult renal tumor Accounts for approximately 3% of all newly diagnosed malignancies in the US Accounts for 85% of all renal malignancies 2:1 male predominance Smoking is the most significant risk factor Usually a solitary, unilateral tumor Propensity for the poles Tendency to invade the renal vein

Answer 55

Classic triad Costovertebral pain, palpable mass, and hematuria All three are only seen in about 10% of cases Hematuria is most reliable but often intermittent Often silent, large (10 cm), and metastatic at diagnosis 5 year survival is from 60-90% Treatment is nephrectomy and chemotherapy

Answer 56

WAGR syndrome Denys-Drash syndrome Beckwith-Weidemann syndrome

Renal Pathology Flashcards

(80 cards)