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DT III > Renal NV > Flashcards

Renal NV Flashcards

1
Q

Which structure is seen in the renal cortex but absent in the renal medulla?

A

Glomeruli

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2
Q

Azotemia?

describe 3 types

A

Elevation of BUN and Cr related to decr GFR;
Pre-renal:Hypoperfusion of kidneys impairing renal fxn in absence of renal parenchymal damage (ie due to hypovolemic shock, CHF..);
Postrenal: obstruction of urine flow downstream of kidney (ie Ureteral stone, BPH..);
Renal: from Intrinsic renal disease

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3
Q

Uremia

A

When renal failure causes clinical S/Sx in other systems (such as Fibrinous pericarditis)

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4
Q

Rapidly Progressive Glomerulonephritis?

A

Nephritic syndrome w rapid decline of GFR

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5
Q

Asymptomatic hematuria and/or proteinuria is due to?

A

mild glomerular abnormalities

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6
Q

Chronic Kidney Disease

A

GFR less than 60 for atleast 3 mos; end result of all chronic renal parenchymal diseases

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7
Q

End-stage renal disease?

A

GFR less than 5% of normal, chronic dialysis required

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8
Q

Acute kidney injury?

A

Rapid decline in GFR (hrs to days), in severe cases may have oliguria or anuria; Azotemia; frequently reversible

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9
Q

if only some glomeruli are affected by a certain disease and only part of each affected glomerulus is involved, the extent of involvement is described as?

A

Focal (only some glomeruli affected) Segmental (part of the glomerulus is affected)

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10
Q

Extent of involvement: Diffuse?

A

ALL the glomeruli are affected by the disease

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11
Q

Global involvement means?

A

within an individual glomerulus, all of the glomerulus is affected by disease

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12
Q

what 3 methods are used to examine renal diseases?

A

Light microscopy (disease process/devel.); Immunofluorescence (etiology); EM (structural alterations)

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13
Q

What 4 stains are used in light microscopy to highlight components of the glomerulus?

A

PAS, Trichrome, H and E, Silver

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14
Q

Most kidneys lose fetal lobulations in early childhood, what is clinical sign. if they persist into adulthood?

A

none

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15
Q

Bilateral vs Unilateral Agenesis of the kidney?

A

Bilateral- incompatible w life; Unilateral- normal life expectancy, may see compensatory hypertrophy of existing kidney and may develop progressive glomerulosclerosis leading to CKD

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16
Q

Since the kidney produces much of the amniotic fluid via urine, fetal renal disease or bilateral renal agenesis/dysgenesis will often lead to? if amniotic fluid is greatly reduced ->

A

Oligo- or poly- hydramnios;
fetal compression, Potter Facies, positioning defects in hands/feet, Breech position and pulmonary hypoplasia that is lethal

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17
Q

Name some conditions that are risky in pts. w Unilateral Renal agenesis

A

any disease w potential for renal damage ie. pregnancy, DM, HTN; as well as chemo, any renal parenchymal disease..

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18
Q

Congenital Kidney Hypoplasia? It may be difficult to distinguish this from what?

A

Failure of kidney(s) to develop to a normal size; Unilateral (more common) or bilateral (early childhood renal failure);
An acquired small kidney due to atrophy from a systemic disease (ie HTN)

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19
Q

How is Horseshoe kidney usually discovered?

Which poles are fused 90% of the time?

A

Typically ASx and incidentally found by CT or US or at autopsy;
Lower (Ant. to great vessels)

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20
Q

Pathogenesis of ADPKD?

A

Mutations in polycystin 1 or 2 -> defects in cell-cell and cell-matrix intxns -> Altered tubular epithelial growth/ differentiation -> Cell prolif., fluid secretion, abnormal extracell. matrix –> Cyst -> interstitial inflamm/fibrosis and Vascular damage

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21
Q

Name 2 genes inv. in devel. of ADPKD, the chromosome each is on and the protein encoded by each

A

the gene PKD1 on Chr 16p encodes polycystin-1;
PKD2 on Chr 4 encodes polycystin-2
(both of these are integral mem. proteins)

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22
Q

A mutation in which gene: causes most cases of ADPKD?

Causes the more severe disease?

A

PKD1 (85%) ;
PKD1 (avg age of onset of ESRD is 53yrs)
(vs PKD2 avg age of onset of ESRD is 69yrs)

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23
Q

Morphology of kidney in ADPKD?
where do cysts arise?
Microscopically will see?

A

Greatly enlarged kidneys (palpable on PE), external surface covered w cysts;
Arise from tubules throughout the nephron ;
Functioning nephrons btwn the cysts

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24
Q

ADPKD may by ASx until later in disease when pts develop S/Sx of renal insuff., what may cause pain in these pts?

A

Expanding cysts, passing blood clots (hemorrhage into cysts -> hematuria)

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25
Q

3 extrarenal lesions that may be seen in pts w ADPKD?

A

Hepatic cysts (40% of pts), Berry Aneurysms, Cardiac valve anomalies

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26
Q

Name Gene inv. in devel. of ARPKD, the Chr., and the protein encoded by the gene; what age group is affected?

A

PKHD1, Chr 6 (p21-p23), Fibrocystin (fxn unknown);

Pediatric

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27
Q

ARPKD Morphology

A

Enlarged kidneys, external surface is smooth, cut surfaces are sponge-like bc of numerous dilated elongated longitudinal cysts arising from collecting ducts, cysts in cortex and medulla, liver cysts

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28
Q

What extrarenal organ is almost always affected in ARPKD?

A

liver- almost always has cysts, may have periportal fibrosis which -> liver compromise/cirrhosis in childhood of pts who survive past the neonatal period

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29
Q

4 categories of ARPKD? which are the most common?

A

Perinatal, neonatal, infantile, juvenile

Perinatal and neonatal (born w enlarged/cystic kidneys -> early death)

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30
Q

A radiologist sees a single renal lesion on CT performed for staging a colon Ca. what clues help distinguish it as cyst rather than another Ca. or metastasis?

A

Cyst will have smooth edges, avascular, fluid signal rather than solid signal (they are filled w clear serous fluid)

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31
Q

Name one possible serious complication of acquired (dialysis-assoc.) cystic renal disease

A

Renal cell carcinoma, develops in cyst wall (rare- 7% of pts.)

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32
Q

Describe the cysts seen in acquired (dialysis-assoc.) cystic renal disease after prolonged dialysis
These cysts likely develop due to?

A

Numerous cortical and medullary cysts 0.5-2cm , clear fluid contents, may contain Ca++ oxalate crystals, usually ASx;
Tubular obstruction by fibrosis or oxalate crystals

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33
Q

Name 2 renal cystic diseases that affect kids?

Which is the MC cause of genetic renal disease in kids/ young adults? (in bold)

A

ARPKD and Nephronophthisis

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34
Q

Nephronophthisis may cause what extra-renal clinical features?

A

EOM motor abnormalities, Retinal dystrophy, Cerebellar abnormalities, Liver fibrosis

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35
Q

Simple Renal cysts

A

Single or multiple, cortical , 1-5cm, common, increase w age, microscopic hematuria OR ASx, not clinically sign. BUT must distinguish from tumors on imaging, NOT genetic

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36
Q

Multicystic Renal Dysplasia

A

Congenital anomaly, Cystic, various sizes; Islands of undiffer. mesenchyme, cartilage, immature CDs; Unilateral (surgically remove affected kidney) or Bilateral (renal failure develops)

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37
Q

Small kidneys w granular surface; 1st Sx: Polyuria/ polydipsia, unable to concentrate urine; Na+ wasting and tubular acidosis, progresses to terminal renal failure in 5-10yrs? why is this difficult to diagnose?

A

Nephronophthisis; cysts are too small to see on imaging

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38
Q

Nephronophthisis: where in the kidney do the cysts occur? What changes are seen in the cortex?
leads to?

A

Corticomedullary jxn;
Tubular atrophy, thickening of the BM of proximal and distal tubules, interstitial fibrosis ;
renal insuff., CRF, ESRD

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39
Q

Nephronophthisis is a group of progressive renal disorders, AD or AR? 3 variants?
which is MC? 3 genes inv. in the MC variant?

A

AR; Sporadic nonfamilial, Familial juvenile, Renal-retinal dysplasia;
Familial juvenile is MC, invs NPH1, NPH2, NPH3;

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40
Q

Medullary Sponge Kidney

A

Adults, All cysts in medulla, cystic dilations of collecting ducts; usually ASx but may result in hematuria, infection, urinary calculi; renal fxn is not affected

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41
Q

Cortical and medullary Collecting tubules and medullary CDs arise from?

A

Ureteric bud

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42
Q

glomerulus, proximal/distal Convoluted tubules, loops of henle, and CT of renal interstitium arise from?

A

Metanephric blastema

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43
Q

Tip of Renal Pyramid=

A

Renal papilla

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44
Q

Loop of henle is in what part of the kidney?

A

Medulla

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45
Q

Why do proximal tubules have more vague/irregular lumen histologically vs crisp border of distal tubule lumen

A

Proximal tubules have long villi

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46
Q 
MC cause (85%) of Intrinsic ARF? 
other causes?
A

Acute Kidney Injury(AKI)/Acute tubular necrosis(ATN);

Acute interstitial nephritis, Glomerulonephritis, thromboembolism

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47
Q

MC causes of AKI/ATN? name 3 other causes

A

Ischemia and Toxic injury

DIC, Obstruction, acute tubulointerstitial nephritis

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48
Q

EARLY micro features of AKI/ATN: varies from..

A

cell swelling to focal tubular epithelial necrosis and apoptosis w desquamation of cells into lumen; dilated PTs w thinning/loss of PAS+ brush border ; casts in distal and CDs, eosinophilic hyaline casts of Tamm-Horsfall protein ; WBCs in dilated vasa recta, interst. edema

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49
Q

Late micro features of AKI/ATN:

A

Epithelial regeneration (flattened epithelium, dilated tubular lumen, large dark nuclei w prominent nucleoli and mitotic figures)

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50
Q

MC cause of Acute pyelonephritis?

A

E. coli (G- bacilli)

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51
Q

Clinical signs of Acute pyelonephritis?

A

Systemic signs of infection ie fever, pain, malaise; Costovertebral angle tenderness, WBC CASTS in urine is diagnostic

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52
Q

What histo changes will you see with Polyoma virus Nephropathy? what will you see under EM?

A

kidneys show enlarged tubular epithelial cells with nuclear inclusion and interstitial inflammation;
intranuclear viral inclusions described as “Crystalline-like lattices”

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53
Q

Thyroidization?

A

the kidney looks like a thyroid tissue, tubular atrophy and dilation; seen in Chronic pyelonephritis

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54
Q

Chronic pyelonephritis from Reflux nephropathy vs Chronic Obstructive pyelonephritis?

A

Vesicouretral Reflux: more common, early childhood, the scars are polar assoc. w underlying blunted calyces, fibrosis;
Diffuse or localized Obstruction- causes fibrosis and blunted calyces all over the kidney

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55
Q

Chronic tubulointerstitial disease w gross, irregular asymmetric scars, assoc. w anatomic abnormality, Histo- see Lymphocytes, plasma cells, interstitial fibrosis and Thyroidization

A

Chronic pyelonephritis

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56
Q

Treatable interstitial disease if recognized early, often begins ~15 days after exposure to synthetic PCNs (meth-/amp-icillin), rifampin, thiazide diuretics or NSAIDs, etc. ? Will see an increase in what cells around tubules?

A

Drug-Induced Interstitial Nephritis;

Eosinophils

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57
Q

If you see gross Papillary Necrosis at various stages (areas of pale gray necrosis limited to papillae) it is likely due to?

A

Chronic heavy use of phenacetin analgesics –> Analgesic Nephropathy

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58
Q

Multiple Myeloma= Plasma cell neoplasm, invs. skeleton at multiple sites (punched out lesions), abundance of IgA and IgG, assoc. w primary amyloidosis and what kidney disease?

A

Multiple Myeloma Renal disease: tubulointerstitial disease, Light chain casts obstructing tubules, Bence-Jones proteins, inflamm. rxn w giant cells around tubular casts; Nephrocalcinosis, see spike in M protein, Conga Red stain +, apple-green birefringence

59
Q

Xanthogranulomatous Pyelonephritis is a benign inflamm. disease that is caused by what? is easily confused with ?

A

Proteus Infections and obstructions;

Renal Cell carcinoma

60
Q

Dilation of renal pelvis/calyces with progressive atrophy of kidney due to obstruction to urine flow?

A

Hydronephrosis

61
Q

Main 4 types of renal Calculi? (in order from MC to least)

A

1) Ca++ oxalate and phosphate (MC, 70%); 2) Struvite; 3) Uric Acid; 4) Cystine (genetic defects in renal absorption of AA, cystinuria)

62
Q

Assoc. w urea-splitting bacteria (mainly proteus, some staph) that convert urea to Ammonia -> Alkaline urine causes precipitation of stones?

A

Mg++ Ammonium phosphate stones AKA Triple Stones/Struvite; Staghorn Calculi; (these are the only type of stones that form in alkaline pH!)

63
Q

Acute Cellular Rejection? Tx?

A

occurs in days-wks, T-cell mediated, interstitial mononuclear cells/lymphocyte infiltration (foamy histiocytes), thickened vessels, fibroblasts, edema, parenchymal injury;
Promptly responds to increased immunosuppressive therapy

64
Q

Acute Humoral Rejection? Tx?

A

occurs in days-wks, Assoc. w necrotizing vasculitis, see neutrophils, fibrin, and thrombin, deposition of C4d;
Tx w B cell depleting agents

65
Q

Renal Papillary Adenoma

A

Small Benign tumor **

66
Q

Benign tumor cmpsd of thick walled blood vessels, smooth m. and fat, incs spindle and epithelioid cells, usually one large mass? multiple masses suggests what?

A

Angiomyolipoma (usually in adults);

Tuberous sclerosis AD, LOF of the tumor suppressor genes TSC1 on Ch 9q or TSC2 on Ch 16

67
Q

MC type (70-80%) of RCC ? 98% of these tumors have?

A

Clear cell type (see clear cytoplasm); Loss of sequs of the short arm of Ch 3 this region has VHL gene which is why RCC seen in pts w VHL Syndrome

68
Q

Papillary Type RCC

A

Papillary growth pattern w histiocytes, usually multifocal, somoma bodies, can be assoc. w dialysis; Sporadic- Trisomies of Chs 7, 16, 17 or loss of Y in males;
Familial- Trisomy 7 =locus for MET

69
Q

Chromophobe Type RCC histo?

A

Distinct cell memb, pale eosinophilic cytoplasm, Halo around nucleus, abundant cytoplasm, solid sheets w perinuclear clearing

70
Q

Grossly you see well-demarcated, mahogany-brown, 6.5cm mass with central stellate scar, what will you see microscopically? malignant or benign?

A

Oncocytic cells w eosinophilic cytoplasm (it is an Oncocytoma)
Benign

71
Q

35 YOM awakened by severe lower ab pain, radiates to groin, intense pain comes in waves, blood in urine next morning, most likely Dx?

A

Uretetral lithiasis

72
Q

51 YOF recurrent UTI 15 yrs, Proteus mirabilis cultured on several occasions, past 4 days burning pain on urination, rt CV angle tenderness on deep palpation, UA pH 7.5, Dx?

A

Staghorn Calculus (Mg++ ammonium phosphate stones/Struvite)

73
Q

4yo complaining of ab pain for past month, palpation of ab shows a tender mass on the right, lab shows hematuria, CT shows a 12cm circumscribed solid mass in R kidney and nephrectomy performed. Dx? histo? assoc. w what syndromes?

A 
Wilms tumor (4th MC peds malignancy, Dx at ~2-5yrs old); 
Classic triphasic combo: Blastemal cells, Stromal cells and epithelial type cells ;
WAGR (WT1 or PAX6 deletion both on Ch 11), Denys-Drash (WT1 gene), and BWS
74
Q

19 YOF received cadaveric renal transplant, 1mo later rising Cr and BUN, renal biopsy performed, Txed w steroids and renal fxn improved, what did the biopsy show?

A

Interstitial infiltration by CD3+ lymphocytes and tubular epithelial damage (Acute Cellular rejection)

75
Q

Hyperacute rejection

A

mins-hrs, cyanotic, molted flaccid kidney, Ag-Ab rxn at level of vascular endothelium, thrombus formation! ; Micro: Fibrin, thrombi and WBC, remove the nonfxning kidney

76
Q

Chronic rejection? does it respond to standard immunosupp. regimen?

A

months-yrs, progr. increase in serum Cr, Hyalinization of glomeruli, interstitial fibrosis and tubular atrophy, focal hemorrhage, swollen kidney, SMCs and CT in vessel intima; No

77
Q

Benign, well circumscribed, gray-white firm nodule,

A

Renal Fibroma ; Fibroblast like cells, collagenous tissue and entrapped tubules at periphery

78
Q

Fine cysts in mucosa cmpsd of dilated Brunn nests (1-5mm in diameter)

A

Ureteritis cystica

79
Q

Fine granular mucosa due to lymphoid follicles

A

Ureteritis follicularis

80
Q

Majority of malignant tumors arising from ureters are? assoc. w ?

A

Urothelial carcinomas; smoking, occupational exposure (arylamines), analgesic nephropathy, HNPCC (mutation in DNA mismatch repair gene, detected by MSI)

81
Q

What type of extrinsic obstructive lesion can be assoc. w IgG4-related disease?

A

Sclerosing retroperitoneal fibrosis

82
Q

Development failure of Ant. wall of abdomen and bladder

A

Exstrophy

83
Q

Interstitial Cystitis (Chronic Pelvic pain syndrome) is a painful/persistent chronic cystitis, fibrosis of bladder wall, likely autoimmune origin, compare its phases

A

Early- Submucosal hemorrhage noted;

Late- classic, ulcerative phase (Hunner ulcers), chronic mucosal hemorrhage noted

84
Q

Special form of inflamm. in bladder related to chronic bacterial infections (mostly E.coli, Proteus), defect in phagocytosis, flat plaques? characteristic finding?

A

Malacoplakia; Michaelis-Gutmann bodies (dense round bodies- laminated mineralized concretions, Ca++ in lysosomes)

85
Q

Nephrogenic metaplasia/adenoma ?

A

Benign response to injury, cuboidal epithelium and tubular proliferation of lamina propia; may be confused w cancer

86
Q

Molecular genetics assoc w Bladder tumors?

A

GOF of FGFR3 (low grade); LOF of TP53 and RB (high grade); activating mutation of HRAS oncogene; loss of genetic material on Ch 9

87
Q

58 YO moves from Egypt and presents w large bladder mass, likely has infection with? which is a major risk for what ?

A

Schistosoma (histo- can see eggs); SCC

88
Q

Botyroid rhabdomyosarcoma?

A

Grape-like, m. origin, cambium layer (superficial layer of tumor looks darker bc more tumor cells), deeper hypocellular and myxoid(mucinous) stroma, sheets of blue cells; seen in infancy or kids

89
Q

Reiter syndrome?

A

Type of reactive arthritis- arthritis, conjunctivitis, urethritis
(can’t see, can’t pee, can’t climb a tree)

90
Q

Origin of tumors arising from proximal vs distal Urethra?

A

Proximal- Urothelial;

Distal: squamous cell

91
Q

Normal ureters have narrowing at?

A
  1. Ureteropelvic jxn (can be obstructed in infants); 2. Crossing at external/common iliac artery
  2. where ureters enter bladder (enter in an oblique manner)
92
Q

3 congenital anomalies of the ureters?

A

double ureters (assoc. w duplication of renal pelvis), Ureteropelvic jxn obstruction (kids, boys, left, hydronephrosis) ; and Diverticula (saccular outpouching of ureteral wall)

93
Q

Abnormalities in [Na+], the major extracellular cation, reflect problems with ?
Values of hypo-/hypernatremia?

A

free water handling (do NOT represent excess/deficiency of Na+); hypo is Na+ less than 135; hyper is greater than 145meq/L

94
Q

90% of pts w this electrolyte abnormality are elderly or chronically ill without ability to drink water

A

Hypernatremia (too little free H2O, often not clinically sign until >150meq/L)

95
Q

Hypernatremia: clinical features?

to diagnose, measure?

A

pts may feel weak and thirsty, tachycardia or low BP may be present, skin turgor may be poor, mucous membranes dry; Urine osmolality

96
Q

How would you expect the urine to be if pt. hypernatremic?

exception?

A

pts. w free H2O depletion will excrete concentrated urine in effort to conserve H2O (=high urine osmolality);
pts w Diabetes Insipidus, w absence of ADH (or its effect) have hypernatremia and DILUTE urine

97
Q

hypernatremia Tx?

A

The unstable pt. should be given IV fluids to stabilize BP; Calc. free H2O deficit and correct this w hypotonic fluids over a 48hr period!

98
Q

clinical features hyponatremia

A

usually no Sx or finding. nausea, fatigue, confusion, neurological deficits may occur esp w levels less than 120

99
Q

what is a surrogate for ADH activity?

a surrogate for vol status?

A

Urine osmolality;

Urine Na+

100
Q

cause of hyponatremia is based on vol status: causes of hypovolemic hyponatremia? Tx?

A

Diuretics and other causes of volume loss ; IV fluids to restore vol if they show S/Sx of sign vol depletion

101
Q

cause of euvolemic hyponatremia? Tx?

A

SIADH -[small cell lung ca. (ectopically produces ADH) and SSRIs can cause SIADH]; fluid restriction

102
Q

causes of hypervolemic hyponatremia?

A

CHF, cirrhosis, and nephrotic syndrome

103
Q

Pts w Sxs attributable to hyponatremia itself should be given?

A

hypertonic saline carefully! to get Na+ > 120 or until seizures stop (correction beyond this is very dangerous), avoid correcting > 8-10meq/L in 24hrs

104
Q

hyponatremia diagnosis?

A

thorough H and P, assess overall vol status!, get urine osmolality and urine Na+

105
Q

If pt has significant hyponatremia (less than 125) would expect urine osmolality to be ??!

A

very low, ADH should be suppressed thus urine should be maximally dilute

106
Q

K+ is major intracellular cation, very little of the body’s K+is in circulation and it shifts across cell membs w pH changes which can cause marked ______ during acidemia and _____ during alkalemia

A

hyperkalemia;

hypokalemia

107
Q

Hyperkalemia: value? causes? commonly seen in what conditions?

A

K+ > 5.0meq/L; excessive intake (esp when excretory ability is compromised), acidosis, lack of Aldo effect, severe vol depletion and drugs (ie K+ sparing diuretics like spironolactone) ;
ARF and CRF

108
Q

Hyperkalemia usually has no history or physical findings, but in acute or severe cases may see what? if present then?

A

conduction abnormalities on EKG; administer calcium gluconate (since these reflect inc risk for arrhythmia)

109
Q

Why should you repeat blood test if results show Hyperkalemia in unsuspected pt. ?

A

to rule out hemolysis as a cause (from lysed RBCs in the tube)

110
Q

Hyperkalemia Tx?

A

decrease serum K+ using insulin and albuterol (shift K+ into cells, transient); give K+ binding resin to increase excretion; Hemodialysis may be needed in ARF

111
Q

Hypokalemia: value? causes? Sx?

A

K+ less than 3.5; K loss from diarrhea, diuretics, Mg++ deficiency!!!!, alkalemia; muscle twitching/weakness, arrhythmia risk in pts w heart disease

112
Q

hypokalemia Tx?

A

give Oral K+ if possible since IV KCl can cause vein irritation and sclerosis, admin. in boluses (such as 40meq at a time) to avoid excessive rises in serum conc.

113
Q

Mg++ is a cofactor for cellular ATPases, deficiency seen in? low Mg++ can lead to?

A

alcoholics, pts. w CKD, and pts on diuretics (loops) ;
Refractory hypokalemia
(Avoid Mg++ loading in pts w renal disease)

114
Q

Measurement of random urine K+ is not routinely useful so what can be done to Dx hypokalemia?

A

EKG can be checked for lengthening of QTc; also check Mg++ level bc low Mg makes correction of K very difficult! if low Mg must be replaced before K+ supplementation will be effective

115
Q

Normal pH of blood? blood pH is determined by the levels of what in plasma? H-H equation?

A

7.4; carbonic acid and bicarb;

pH= pKa + log [A-]/[HA]

116
Q

ARF ? divided into?

A

sudden decrease in renal fxn; Prerenal (decreased perfusion, metabolic derangements, sepsis, hypovolemia, diuretics, BP meds, hypercalcemia..); Postrenal (Obstruction- tumors. BPH, clots); and Intrinsic

117
Q

Dx of ARF

A

careful H/P (H: ask meds, reasons to be vol depleted, h/o kidney probs, Sx?; P: vol status!!!, BP, signs of HF or uremia?, check prostate); Urinalysis/Micro exam of urine!!, BUN/Cr ratio, FENa, US or CT if obstruction suspected!

118
Q

Urinalysis- evaluate for?

A

WBCs, RBCs, Casts, crystals, urine pH, Pigment, protein

119
Q

Both BUN and Cr can be “falsely” low in pts with?

FENa is difficult to interpret in what pts?

A

cirrhosis, cachexia, or severe protein malnutrition;

those taking diuretics or w CKD (pts w CKD typically never have FENa less than 1)

120
Q

Prerenal ARF features

A

FENa less than 1, BUN/Cr ratio greater than 20:1 and elevated Cr and oliguria suggest renal under-perfusion thus under-filtration of blood; common!, usually reversible but if not Txed –> AKI

121
Q

postrenal azotemia

A

obstruction!, suspect clinically- pain and hyperkalemia often present; causes inc enlarged prostate, stones, ureteral compression, clots

122
Q

Intrinsic renal disease includes?

A

AKI/ATN (responsible for 85-90%of cases), Glomerulonephritis, Interstitial nephritis, and Atheroembolic renal disease

123
Q

Intrinsic renal disease features

A

BUN/Cr usually less than 20:1, cmplx interplay of factors leading to tubular cell injury and death; Cr and urine flow are LATE markers but they are the best we have

124
Q

AKI

A

end organ dysfxn in which diffuse inflamm leads to impaired renal perfusion; this will be the end result if prerenal azotemia not Tx; frequ accompanies SIRS/Sepsis, can be induced by rhabdomyolysis or contrast

125
Q

acute Glomerulonephritis features? exs?

A

“Nephritic” sediment with WBC casts, proteinuria, and dysmorphic RBCs; HTN may be present, look for other systemic signs of disease, FENa usually less than 1 %

126
Q

Typically assoc w meds (ABX, NSAIDs), rise in Cr occurs several wks after exposure, may see: eosinophil -ia/-uria , rash, fever; not common

A

Interstitial nephritis (BUN/Cr ratio less than 20:1)

127
Q

Atheroembolism

A

atherosclerotic debris embolizes in the renal vessels, usually after a vascular procedure, pt. usually has PAD, purple toes, unremarkable urine sediment, complement levels usually low

128
Q

Rhabdomyolysis features? causes? Tx?

A

Severe m. injury will lead to myoglobinuria -urine has red color but no RBCs and RF, elevated CPK, m. pain;
Crush injuries, m. injury from fall, occurs rarely w statin use;
Vigorous hydration!! may need dialysis

129
Q

Tubular injury from hyperosmolar contrast medium ?
what pts MAY be more susceptible?
what MAY be somewhat protective?

A

contrast induced AKI -> Unremarkable sediment!!;
those w diabetes/myeloma;
premedication (acetylcysteine) and hydration

130
Q

Drug/toxin induced AKI from what drugs?

A

meds such as diuretics, ACE-I, NSAIDs are vasoactive and may be deleterious during acute renal decompensation; Other drugs nephrotoxic (cisplatin, amphotericin, aminoglycosides) - tubular toxins
Drug dosing may need adjusted during ARF!!

131
Q

Drug/toxin induced AKI from what toxins?

A

Poisoning by heavy metals (mercury..); ethylene glycol (causes accum of Ca oxalate crystals!!) and methanol are toxic alcohols- elevate anion gap, cause RF due to breakdown products

132
Q

Pts w oliguric ARF may quickly develop what conditions and need immediate dialysis?

A

hyperkalemia and acidemia

133
Q

60 YOF presents w N/V/D for 4 days and is now very weak. Meds inc a diuretic and ACEi for BP. BP is 80/60. BUN/Cr are 44/1.9.
Likely cause? initial Tx? what do you expect FENa to be?***

A

prerenal azotemia (could be due to her vasoactive meds);
Should first give IV fluids!;
FENa would likely be less than 1%

134
Q

30 YOM presents w weakness/confusion, h/o IV drug abuse, temp 104, BP 70/50 HR 130, BUN/Cr 50/3.3, pulses weak. likely cause of RF? initial Tx? what do you expect FENa to be?

A

AKI from sepsis (ratio is less than 20:1; obstruction unlikely at this age)
FENa likely GREATER than 1%!!! (not prerenal!)

135
Q

when is a renal tumor w papillary growth pattern (finger like projections):
clearly benign?

A

when less than 0.5cm, tubulopapillary archit.!!!! (and “prob. benign” if like this and up to 1cm)
malignant if greater than 1cm !!! (and prob malignant if less than 1 cm but has solid growth patter, clear cells)

136
Q

primary renal tumor that is stage 4 means

A

tumor invades beyond Gerota’s fascia

137
Q

Aggressive renal tumor w Hobnail type cells (nucleus protruding), tubulopapillary archit. w desmoplastic stroma, poor prognosis, doesnt respond well to chemo?

A

Collecting duct (Bellini duct) carcinoma (malignant)

138
Q

RCC 5 year survival is?

TOC?

A

45-70%, but T3-T4 tumors ~15%;

Nephrectomy

139
Q

Urothelial carcinomas of Renal pelvis account for 5-10% of primary renal tumors, clinical Sx?
They arise from?

A

Hematuria, Hydronephrosis (block outflow), Flank pain;
urothelium of renal pelvis
(histo similar to bladder tumors and prognosis is poor when cancer is invasive/high grade)

140
Q

Syndrome characterized by gonadal dysgenesis, early-onset nephropathy (mesangial sclerosis), defect in DNA binding properties? what gene?

A

Denys-Drash; WT1 gene (90% fisk for Wilms tumor)

141
Q

RCCs arise from renal tubular epithelium, major risk factors?

A

TOBACCO!!, obesity, HTN..

142
Q

RCCs mostly sporadic, 4% familial assoc w what hereditary syndromes?

A

Von-Hippel-Lindau on Chr3; Leiomyomatosis (mutated FH gene); mutation in MET -papillary ca; Birt-Hogg-Dube (AD, BHD gene)

143
Q

at presentation 25% of RCC have mets, 2 MC sites?

A

lungs then bones

DT III (2 decks)

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