Renal NV Flashcards
1
Q
Which structure is seen in the renal cortex but absent in the renal medulla?
A
Glomeruli
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
3
Q
Uremia
A
When renal failure causes clinical S/Sx in other systems (such as Fibrinous pericarditis)
4
Q
Rapidly Progressive Glomerulonephritis?
A
Nephritic syndrome w rapid decline of GFR
5
Q
Asymptomatic hematuria and/or proteinuria is due to?
A
mild glomerular abnormalities
6
Q
Chronic Kidney Disease
A
GFR less than 60 for atleast 3 mos; end result of all chronic renal parenchymal diseases
7
Q
End-stage renal disease?
A
GFR less than 5% of normal, chronic dialysis required
8
Q
Acute kidney injury?
A
Rapid decline in GFR (hrs to days), in severe cases may have oliguria or anuria; Azotemia; frequently reversible
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)
10
Q
Extent of involvement: Diffuse?
A
ALL the glomeruli are affected by the disease
11
Q
Global involvement means?
A
within an individual glomerulus, all of the glomerulus is affected by disease
12
Q
what 3 methods are used to examine renal diseases?
A
Light microscopy (disease process/devel.); Immunofluorescence (etiology); EM (structural alterations)
13
Q
What 4 stains are used in light microscopy to highlight components of the glomerulus?
A
PAS, Trichrome, H and E, Silver
14
Q
Most kidneys lose fetal lobulations in early childhood, what is clinical sign. if they persist into adulthood?
A
none
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
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
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..
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)
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)
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
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)
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)
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
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)
25
3 extrarenal lesions that may be seen in pts w ADPKD?
Hepatic cysts (40% of pts), Berry Aneurysms, Cardiac valve anomalies
26
Name Gene inv. in devel. of ARPKD, the Chr., and the protein encoded by the gene; what age group is affected?
PKHD1, Chr 6 (p21-p23), Fibrocystin (fxn unknown);
| Pediatric
27
ARPKD Morphology
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
28
What extrarenal organ is almost always affected in ARPKD?
liver- almost always has cysts, may have periportal fibrosis which -> liver compromise/cirrhosis in childhood of pts who survive past the neonatal period
29
4 categories of ARPKD? which are the most common?
Perinatal, neonatal, infantile, juvenile
| Perinatal and neonatal (born w enlarged/cystic kidneys -> early death)
30
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?
Cyst will have smooth edges, avascular, fluid signal rather than solid signal (they are filled w clear serous fluid)
31
Name one possible serious complication of acquired (dialysis-assoc.) cystic renal disease
Renal cell carcinoma, develops in cyst wall (rare- 7% of pts.)
32
Describe the cysts seen in acquired (dialysis-assoc.) cystic renal disease after prolonged dialysis
These cysts likely develop due to?
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
33
Name 2 renal cystic diseases that affect kids?
| Which is the MC cause of genetic renal disease in kids/ young adults? (in bold)
ARPKD and **Nephronophthisis**
34
Nephronophthisis may cause what extra-renal clinical features?
EOM motor abnormalities, Retinal dystrophy, Cerebellar abnormalities, Liver fibrosis
35
Simple Renal cysts
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
36
Multicystic Renal Dysplasia
Congenital anomaly, Cystic, various sizes; Islands of undiffer. mesenchyme, cartilage, immature CDs; Unilateral (surgically remove affected kidney) or Bilateral (renal failure develops)
37
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?
Nephronophthisis; cysts are too small to see on imaging
38
Nephronophthisis: where in the kidney do the cysts occur? What changes are seen in the cortex?
leads to?
Corticomedullary jxn;
Tubular atrophy, thickening of the BM of proximal and distal tubules, interstitial fibrosis ;
renal insuff., CRF, ESRD
39
Nephronophthisis is a group of progressive renal disorders, AD or AR? 3 variants?
which is MC? 3 genes inv. in the MC variant?
AR; Sporadic nonfamilial, Familial juvenile, Renal-retinal dysplasia;
Familial juvenile is MC, invs NPH1, NPH2, NPH3;
40
Medullary Sponge Kidney
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
41
Cortical and medullary Collecting tubules and medullary CDs arise from?
Ureteric bud
42
glomerulus, proximal/distal Convoluted tubules, loops of henle, and CT of renal interstitium arise from?
Metanephric blastema
43
Tip of Renal Pyramid=
Renal papilla
44
Loop of henle is in what part of the kidney?
Medulla
45
Why do proximal tubules have more vague/irregular lumen histologically vs crisp border of distal tubule lumen
Proximal tubules have long villi
46
```
MC cause (85%) of Intrinsic ARF?
other causes?
```
Acute Kidney Injury(AKI)/Acute tubular necrosis(ATN);
| Acute interstitial nephritis, Glomerulonephritis, thromboembolism
47
MC causes of AKI/ATN? name 3 other causes
**Ischemia and Toxic injury**
| DIC, Obstruction, acute tubulointerstitial nephritis
48
EARLY micro features of AKI/ATN: varies from..
**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
49
Late micro features of AKI/ATN:
**Epithelial regeneration** (flattened epithelium, dilated tubular lumen, large dark nuclei w prominent nucleoli and mitotic figures)
50
MC cause of Acute pyelonephritis?
E. coli (G- bacilli)
51
Clinical signs of Acute pyelonephritis?
Systemic signs of infection ie fever, pain, malaise; Costovertebral angle tenderness, **WBC CASTS in urine is diagnostic**
52
What histo changes will you see with Polyoma virus Nephropathy? what will you see under EM?
kidneys show enlarged tubular epithelial cells with nuclear inclusion and interstitial inflammation;
intranuclear viral inclusions described as "Crystalline-like lattices"
53
Thyroidization?
the kidney looks like a thyroid tissue, tubular atrophy and dilation; seen in **Chronic pyelonephritis**
54
Chronic pyelonephritis from Reflux nephropathy vs Chronic Obstructive pyelonephritis?
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
55
Chronic tubulointerstitial disease w gross, **irregular asymmetric scars**, assoc. w anatomic abnormality, Histo- see **Lymphocytes, plasma cells, interstitial fibrosis and Thyroidization**
Chronic pyelonephritis
56
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?
Drug-Induced Interstitial Nephritis;
| **Eosinophils**
57
If you see gross Papillary Necrosis at various stages (areas of pale gray necrosis limited to papillae) it is likely due to?
Chronic heavy use of phenacetin analgesics --> Analgesic Nephropathy
58
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?
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
Xanthogranulomatous Pyelonephritis is a benign inflamm. disease that is caused by what? is easily confused with ?
**Proteus Infections** and obstructions;
| Renal Cell carcinoma
60
Dilation of renal pelvis/calyces with progressive atrophy of kidney due to obstruction to urine flow?
**Hydronephrosis**
61
Main 4 types of renal Calculi? (in order from MC to least)
1) Ca++ oxalate and phosphate (MC, 70%); 2) Struvite; 3) Uric Acid; 4) Cystine (genetic defects in renal absorption of AA, cystinuria)
62
Assoc. w urea-splitting bacteria (mainly **proteus**, some staph) that convert urea to Ammonia -> **Alkaline** urine causes precipitation of stones?
Mg++ Ammonium phosphate stones AKA Triple Stones/Struvite; Staghorn Calculi; (these are the only type of stones that form in alkaline pH!)
63
Acute Cellular Rejection? Tx?
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
Acute Humoral Rejection? Tx?
occurs in days-wks, Assoc. w necrotizing vasculitis, see neutrophils, fibrin, and thrombin, deposition of **C4d**;
Tx w B cell depleting agents
65
Renal Papillary Adenoma
Small Benign tumor **
66
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?
Angiomyolipoma (usually in adults);
| **Tuberous sclerosis** AD, LOF of the tumor suppressor genes TSC1 on Ch 9q or TSC2 on Ch 16
67
MC type (70-80%) of RCC ? 98% of these tumors have?
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
Papillary Type RCC
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
Chromophobe Type RCC histo?
Distinct cell memb, **pale eosinophilic cytoplasm**, Halo around nucleus, abundant cytoplasm, solid sheets w perinuclear clearing
70
Grossly you see well-demarcated, mahogany-brown, 6.5cm mass with central stellate scar, what will you see microscopically? malignant or benign?
Oncocytic cells w eosinophilic cytoplasm (it is an Oncocytoma)
Benign
71
35 YOM awakened by severe lower ab pain, radiates to groin, intense pain comes in waves, blood in urine next morning, most likely Dx?
Uretetral lithiasis
72
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?
Staghorn Calculus (Mg++ ammonium phosphate stones/Struvite)
73
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?
```
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
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?
Interstitial infiltration by CD3+ lymphocytes and tubular epithelial damage (Acute Cellular rejection)
75
Hyperacute rejection
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
Chronic rejection? does it respond to standard immunosupp. regimen?
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
Benign, well circumscribed, gray-white firm nodule,
Renal Fibroma ; Fibroblast like cells, collagenous tissue and entrapped tubules at periphery
78
Fine cysts in mucosa cmpsd of dilated Brunn nests (1-5mm in diameter)
Ureteritis cystica
79
Fine granular mucosa due to lymphoid follicles
Ureteritis follicularis
80
Majority of malignant tumors arising from ureters are? assoc. w ?
Urothelial carcinomas; smoking, occupational exposure (arylamines), analgesic nephropathy, HNPCC (mutation in DNA mismatch repair gene, detected by MSI)
81
What type of extrinsic obstructive lesion can be assoc. w IgG4-related disease?
Sclerosing retroperitoneal fibrosis
82
Development failure of Ant. wall of abdomen and bladder
Exstrophy
83
Interstitial Cystitis (Chronic Pelvic pain syndrome) is a painful/persistent chronic cystitis, fibrosis of bladder wall, likely autoimmune origin, compare its phases
Early- Submucosal hemorrhage noted;
| Late- classic, ulcerative phase (Hunner ulcers), chronic mucosal hemorrhage noted
84
Special form of inflamm. in bladder related to chronic bacterial infections (mostly E.coli, Proteus), defect in phagocytosis, flat plaques? characteristic finding?
Malacoplakia; Michaelis-Gutmann bodies (dense round bodies- laminated mineralized concretions, Ca++ in lysosomes)
85
Nephrogenic metaplasia/adenoma ?
Benign response to injury, cuboidal epithelium and tubular proliferation of lamina propia; may be confused w cancer
86
Molecular genetics assoc w Bladder tumors?
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
58 YO moves from Egypt and presents w large bladder mass, likely has infection with? which is a major risk for what ?
Schistosoma (histo- can see eggs); SCC
88
Botyroid rhabdomyosarcoma?
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
Reiter syndrome?
Type of reactive arthritis- arthritis, conjunctivitis, urethritis
(can't see, can't pee, can't climb a tree)
90
Origin of tumors arising from proximal vs distal Urethra?
Proximal- Urothelial;
| Distal: squamous cell
91
Normal ureters have narrowing at?
1. Ureteropelvic jxn (can be obstructed in infants); 2. Crossing at external/common iliac artery
3. where ureters enter bladder (enter in an **oblique** manner)
92
3 congenital anomalies of the ureters?
double ureters (assoc. w duplication of renal pelvis), Ureteropelvic jxn obstruction (kids, boys, left, hydronephrosis) ; and Diverticula (saccular outpouching of ureteral wall)
93
Abnormalities in [Na+], the major extracellular cation, reflect problems with ?
Values of hypo-/hypernatremia?
free water handling (do NOT represent excess/deficiency of Na+); hypo is Na+ less than 135; hyper is greater than 145meq/L
94
90% of pts w this electrolyte abnormality are elderly or chronically ill without ability to drink water
Hypernatremia (too little free H2O, often not clinically sign until >150meq/L)
95
Hypernatremia: clinical features?
| to diagnose, measure?
pts may feel weak and thirsty, tachycardia or low BP may be present, skin turgor may be poor, mucous membranes dry; Urine osmolality
96
How would you expect the urine to be if pt. hypernatremic?
| exception?
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
hypernatremia Tx?
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
clinical features hyponatremia
usually no Sx or finding. nausea, fatigue, confusion, neurological deficits may occur esp w levels less than 120
99
what is a surrogate for ADH activity?
| a surrogate for vol status?
Urine osmolality;
| Urine Na+
100
cause of hyponatremia is based on vol status: causes of hypovolemic hyponatremia? Tx?
Diuretics and other causes of volume loss ; IV fluids to restore vol if they show S/Sx of sign vol depletion
101
cause of euvolemic hyponatremia? Tx?
SIADH -[**small cell lung ca.** (ectopically produces ADH) and SSRIs can cause SIADH]; fluid restriction
102
causes of hypervolemic hyponatremia?
CHF, cirrhosis, and nephrotic syndrome
103
Pts w Sxs attributable to hyponatremia itself should be given?
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
hyponatremia diagnosis?
thorough H and P, assess overall vol status!, get urine osmolality and urine Na+
105
If pt has significant hyponatremia (less than 125) would expect urine osmolality to be ??!
very low, ADH should be suppressed thus urine should be **maximally dilute**
106
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
hyperkalemia;
| hypokalemia
107
Hyperkalemia: value? causes? commonly seen in what conditions?
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
Hyperkalemia usually has no history or physical findings, but in acute or severe cases may see what? if present then?
conduction abnormalities on EKG; administer calcium gluconate (since these reflect inc risk for arrhythmia)
109
Why should you repeat blood test if results show Hyperkalemia in unsuspected pt. ?
to rule out hemolysis as a cause (from lysed RBCs in the tube)
110
Hyperkalemia Tx?
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
Hypokalemia: value? causes? Sx?
K+ less than 3.5; K loss from diarrhea, diuretics, Mg++ deficiency!!!!, alkalemia; muscle twitching/weakness, arrhythmia risk in pts w heart disease
112
hypokalemia Tx?
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
Mg++ is a cofactor for cellular ATPases, deficiency seen in? low Mg++ can lead to?
**alcoholics**, pts. w CKD, and pts on diuretics (loops) ;
**Refractory hypokalemia**
(Avoid Mg++ loading in pts w renal disease)
114
Measurement of random urine K+ is not routinely useful so what can be done to Dx hypokalemia?
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
Normal pH of blood? blood pH is determined by the levels of what in plasma? H-H equation?
7.4; carbonic acid and bicarb;
| pH= pKa + log [A-]/[HA]
116
ARF ? divided into?
sudden decrease in renal fxn; Prerenal (decreased perfusion, metabolic derangements, sepsis, hypovolemia, diuretics, BP meds, hypercalcemia..); Postrenal (Obstruction- tumors. BPH, clots); and Intrinsic
117
Dx of ARF
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
Urinalysis- evaluate for?
WBCs, RBCs, Casts, crystals, urine pH, Pigment, protein
119
Both BUN and Cr can be "falsely" low in pts with?
FENa is difficult to interpret in what pts?
cirrhosis, cachexia, or severe protein malnutrition;
those taking diuretics or w CKD (pts w CKD typically never have FENa less than 1)
120
Prerenal ARF features
**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
postrenal azotemia
obstruction!, suspect clinically- pain and hyperkalemia often present; causes inc enlarged prostate, stones, ureteral compression, clots
122
Intrinsic renal disease includes?
AKI/ATN (responsible for 85-90%of cases), Glomerulonephritis, Interstitial nephritis, and Atheroembolic renal disease
123
Intrinsic renal disease features
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
AKI
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
acute Glomerulonephritis features? exs?
"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
Typically assoc w meds (ABX, NSAIDs), rise in Cr occurs several wks after exposure, may see: eosinophil -ia/-uria , rash, fever; not common
Interstitial nephritis (BUN/Cr ratio less than 20:1)
127
Atheroembolism
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
Rhabdomyolysis features? causes? Tx?
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
Tubular injury from hyperosmolar contrast medium ?
what pts MAY be more susceptible?
what MAY be somewhat protective?
contrast induced AKI -> Unremarkable sediment!!;
those w diabetes/myeloma;
premedication (acetylcysteine) and hydration
130
Drug/toxin induced AKI from what drugs?
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
Drug/toxin induced AKI from what toxins?
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
Pts w oliguric ARF may quickly develop what conditions and need immediate dialysis?
hyperkalemia and acidemia
133
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?***
prerenal azotemia (could be due to her vasoactive meds);
Should first give IV fluids!;
FENa would likely be less than 1%
134
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?
AKI from sepsis (ratio is less than 20:1; obstruction unlikely at this age)
FENa likely GREATER than 1%!!! (not prerenal!)
135
when is a renal tumor w papillary growth pattern (finger like projections):
clearly benign?
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
primary renal tumor that is stage 4 means
tumor invades beyond Gerota's fascia
137
Aggressive renal tumor w Hobnail type cells (nucleus protruding), tubulopapillary archit. w desmoplastic stroma, poor prognosis, doesnt respond well to chemo?
Collecting duct (Bellini duct) carcinoma (malignant)
138
RCC 5 year survival is?
| TOC?
45-70%, but T3-T4 tumors ~15%;
| Nephrectomy
139
Urothelial carcinomas of Renal pelvis account for 5-10% of primary renal tumors, clinical Sx?
They arise from?
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
Syndrome characterized by gonadal dysgenesis, early-onset nephropathy (mesangial sclerosis), defect in DNA binding properties? what gene?
Denys-Drash; WT1 gene (90% fisk for Wilms tumor)
141
RCCs arise from renal tubular epithelium, major risk factors?
TOBACCO!!, obesity, HTN..
142
RCCs mostly sporadic, 4% familial assoc w what hereditary syndromes?
Von-Hippel-Lindau on Chr3; Leiomyomatosis (mutated FH gene); mutation in MET -papillary ca; Birt-Hogg-Dube (AD, BHD gene)
143
at presentation 25% of RCC have mets, 2 MC sites?
lungs then bones
