Renal Flashcards
1
Q
What happens to the pronephros
A
Degenerates at week 4
2
Q
Mesonephros
A
Functions as the interim kidney for 1st trimester. Later contributes to male genital system.
3
Q
Metanephros
A
Appears in 5th week of gestation, nephrogenesis continues through 32-36 weeks.
4
Q
Ureteric bud
A
Derived from the caudal end of the mesonephric duct, develops into the collecting system of the kidney (collecting duct ->ureters).
5
Q
Metanephric mesenchyme
A
Ureteric bud interacts with this tissue to induce differentiation and formation of glomerulus through DCT
6
Q
Uretopelvic junction
A
Last site in kidney to canalize, most common site of obstruction in fetus (causes hydronephrosis).
7
Q
Potter sequence
A
Renal agenesis/ARPKD/posterior urethral valves
lead to oligohydramnios. This causes compression of the developing fetus, especially pulmonary hypoplasia. Also twisted face/skin, micrognathia, low set ears
8
Q
Horseshoe kidney
A
Inferior poles of both kidneys fuse. As they ascend they get caught on the inferior mesenteric artery and remain low in the abdomen. They function normally but increased risk of uretopelvic obstruction, hydronephrosis, renal stones, and rarely wilms tumor.
Associated with turner syndrome
9
Q
Level of the kidneys
A
T12-L3
1,2,3 is where you find the kidneys
10
Q
Multicystic dysplastic kidney
A
Abnormal interaction of the ureteric bud and the metanephric mesenchyme. Nonfunctional kidney with cysts and connective tissue. Bilateral is incompatible with life. Unilateral is asymptomatic.
11
Q
Duplex collecting system
A
Kidney has 2 ureters due to bifurcation of the ureteric bud before interaction with metanephric mesenchyme. Predisposes to UTIs and vesicoureteric reflex (where valve doesnt close when bladder is full. Reflux of urine into ureter.
12
Q
Which kidney is taken during donor transplantation?
A
Left kidney because it has a longer renal vein
13
Q
Course of ureters?
A
Pass under uterine artery and under ductus deferens.
Can be cut during surgeries with ligation of uterine arteries and ovarian arteries.
14
Q
Fluid compartments
A
40 non water
60% water -> 40 intracellular/20extracellular -> 5 plasma/15 interstitium
15
Q
Extracellular fluid measured with?
Plasma volume measured with?
A
Inulin
Albumin
16
Q
Glomerular filtration barrier?
A
Negatively charged due to presence of heparan sulfate. Fenestrated capillary endothelium form size barrier
17
Q
GFR using inulin
A
Calculate using inulin clearance
(UV)/P = clearance of inulin
Normal GFR is 100.
18
Q
Effective renal plasma flow?
A
Calculated using PAH.
RBF can be calculated from RPF using
RPF/(1-HCT)
19
Q
Filtration fraction
A
GFR/RPF
20
Q
Filtered load
A
GFR*plasma concentration
21
Q
Prostaglandin effect on renal vasculature
A
Dilate the afferent arteriole. Increase RPF and GFR, so FF remains constant.
22
Q
Calculation of resorption or excretion
A
Use filtered load and excretion rate
GFRP and UxV
If filtered-secreted is positive, then there is net resorption
23
Q
Glucose clearance
A
Glucosuria begins at 200 mg/dl. Transporters are fully saturated at ~375.
24
Q
Hartnup disease
A
No absorption and high excretion of amino acids (tryptophan), so decreased niacin causing pellagra (dermatitis, dementia, diarrhea).
25
PCT
Reabsorbs sodium, nearly all glucose and amino acids, and most bicarb, chloride, phosphate, K and H2O. Isotonic absorption. Generates and secretes NH3 to buffer the H that is secreted during Na H antiport.
Ang II acts to increase Na H antiporter
PTH acts to inhibit Na PO4 costransport.
Carbonic anhydrase causes H2CO3 to become Co2 and H2O. Co2 enters cell and becomes H2Co3 and allows acid to be regenerated in the lumen.
Blocking carbonic anhydrase causes metabolic acidosis.
26
TAL
Location of the Na K 2Cl cotransporter, K backleak and paracellular transport of Mg and Ca due to positive lumen potential.
27
Distal tubule
Has Na Cl cotransporter, with Ca channel.
PTH increases Na Ca exchanger at the basal membrane. To increase Ca reabsorption.
28
Collecting tubule
Principal cell Na in K out and H2o via aquaporins.
Alpha intercalated cell has H pump
Aldosterone and ADH act on these two cells.
29
Fanconi syndrome
Defective proximal tubule resorption. Associated with excretion of amino acids and glucose. May result in a metabolic acidosis because bicarb can't be resorbed.
Caused by wilson disease, ischemia, nephrotoxins, multiple myeloma
30
Bartter Syndrome
Resorptive defect in thick ascending limb due to an autosomal recessive defect at the na k 2cl transporter. Causes hypokalemia and metabolic alkalosis (because more Na to distal tubule leads to increased H out). Also hypercalciuria (no positive driving force from K backleak).
31
Gitelman Syndrome
Resorptive defect of Na Cl in DCT. Autosomal recessive, less severe than Bartter syndrome. Leads to hypokalemia, hypocalciuria. Also causes metabolic alkalosis. More Na delivery to collecting duct
32
Liddle Syndrome
Increased activity of ENac causes hypokalemia, metabolic alkalosis, hypertension. Autosomal dominant disease. Treat with amiloride.
33
Syndrome of apparent mineralocorticoid excess
Decrease in 11BHSD means much more cortisol around to activate mineralocorticoid receptors. Hypokalemia, hypertension, metabolic alkalosis. Can be caused by licorice
34
TF/P graph
look this up
35
Things that increase renin
Decreased BP sensed in JG cells.
Less Na delivery to macula densa
Increased sympathetic tone (b1 receptors)
36
ANP
Released from atria in states of volume overload. Stimulates cGMP to relax vasculature causing increased GFR and decreased renin. With increased GFR there is no net increase in Na reabsorption so more is lost, decreasing BP.
37
What shifts K into cells
B agonism (albuterol), insulin, hypoosmolarity. Alkalosis
38
What shifts K out of cells
Digitalis, acidosis, b blockers
39
Low Mg can cause...
Torsades, tetany.
40
Things that cause respiratory acidosis
Hypoventilation: airway obstruction, acute lung disease, chronic lung disease, opioids, weakening of respiratory muscles (ALS).
41
Things that cause anion gap metabolic acidosis
MUDPILES
```
Methanol
Uremia
DKA
Propylene glycol
INH or iron
Lactic acidosis
Ethylene Glycol
Salicylates
```
42
Things that causes non gap metabolic acidosis
```
Hyperalimentation
addison disease
RTA
Diarrhea (loss of bicarb and na)
Acetazolamide
spironolactone
saline infusion
```
43
Things that cause respiratory alkalosis
Hyperventilation (hysteria, hypoxemia, salicylates at first, tumor, PE
44
Things that cause metabolic alkalosis
Loop diuretics, vomiting (loss of HCl), antacid use, hyperaldosteronism
45
Renal tubular acidosis type 1
Distal. Defect in the ability of alpha intercalated cells to secrete hydrogen. No HCO3 generated, causes metabolic acidosis with no gap. Associated with hypokalemia (more K out into tubules) and increased risk for calcium phosphate kidneys stones.
Caused by ampho B and congenital abnormalities
46
Renal tubular acidosis type 2
Proximal. Defect in the proximal tubule to resorb HCO3 causes excretion of HCO3 in urine and subsequent metabolic acidosis. Associated with hypokalemia and increased risk for hypophosphatemic rickets. Caused by fanconi syndrome, lead, aminoglycosides, carbonic anhydrase inhibitors.
47
Renal tubular acidosis type 4
Hypoaldosteronism, aldosterone resistance, or K sparing diuretics. More Na in tubules leads to hyperkalemia, impairs ammoniagenesis in the proximal tubule. Decreases the buffering capacity and decreases H excretion into urine.
48
RBC casts
Glomerulonephritis, ischemia, malignany hypertension
49
WBC casts
Interstitial nephritis
50
Fatty casts
oval fat bodies caused by nephrotic syndrome
51
Muddy brown casts
Associated with acute tubular necrosis
52
Waxy casts
Seen in advanced renal disease
53
Hyaline casts
Nonspecific-- can be a normal finding.
54
Nephotic syndrome
>3.5 protein in urine, hypoalbuminemia, hyperlipidemia. Loss of ATIII in urine, loss of immunoglobulin
55
FSGS
Most commonly seen in african americans.
56
Minimal change disease
Happens most commonly in kids. Normal glomeruli but effacement of foot processes on LM. Happens after a viral infection or if Hodgkins lymphoma (due to cytokine production). Responds very well to steroids.
57
Membranous nephropathy
Thickening of capillar and basement membrane. IF granular deposits subepithelial with spike and dome appearance on EM. This is common in SLE. Also most common form in caucasian adults. Can be idiopathic or due to an antibody against phospholipase A2. May progress to chronic renal failure
58
Amyloidosis
Most common site of amyloid deposition. Associated with MM, RA, TB.
59
Diabetic glomerulonephropathy
Mesangial expansion with GBM thickening and kimmelsteilwilson nodules.
Caused by the nonenzymatic glycosylation of the basement membranes. This increases GFR and causes mesangial expansion. Add ace or ARb to protect
60
Membranoproliferative glomerulonephritis
Can present as a nephritic or nephrotic picture.
Type I has subendothelial deposits and tramtrack appearance. Caused by HCV or HBV
Type II is associated with intramembranous immune complex deposits. Caused by C3 nephritic factor that stabilizes C3 convertase, increases complement activation and causes decrease in serum C3 levels.
61
Nephritic syndrome
Inflammatory process that is characterized by RBC casts in urine, azotemia (uremia), oliguria
Caused by Rapidly progressive GN, Alport syndrome, PSGN, IgA, Diffuse proliferative, Membranoproliferative.
62
Rapidly Progressive GN
Seen as a crescent on Light microscopy. Can be caused by a number of things including goodpastures syndrome, GPA, MPA. Crescent is macrophages and fibrin.
Poor prognosis, rapidly deteriorating renal function
63
PSGN
2 or 3 weeks after pharyngitis or skin infection. Type III HSR. Causes enlarged glomeruli and lumby bumpy appearance of immune complex deposition in the subepithelial region.
64
Diffuse proliferative glomerulonephritis
Full house staining on immune staining. Due to SLE. Wire lopping of capillaries. Subendothelial deposits. Most common cause of death.
65
IgA nephropathy
Mesangial expansion with IgA. Seen with henoch schonlein purpura
66
Alport syndrome
Defective type IV collagen synthesis. Glomerulonephritis, deafness, eye problems. X-linked splitting of the basement membrane.
67
Calcium kidney stones
Calcium phosphate if ph high, calcium oxalate if ph low. Radioopaque stones that are envelope or dumbell shaped. Both promoted by hypercalciuria (idiopathic or from increased PTH or cancer). Oxalate crystals can happen from ethalene glycol, vitamin C abuse or crohn's disease. Treat with thiazides and citrate.
Patients frequently are normocalcemic
68
Ammonia Magnesium phosphate stones
15% of stones seen when urine ph is high from ureasepositive bugs like proteus, staph, kleb. Create ammonia. They are coffin lid in shape and are radioopaque.
69
Uric acid stones
When ph decreases. Radiolucent rhomboid stones. Seen when urine volume is down or when uric acid is high (gout, tumor lysis syndrome). Treat by alkalinizing the urine
70
Cystine stones
Radioopaque, hexagonal. Mostly seen in children secondary to cystinuria.
Hydrate and alkalinize the urine.
71
Hydronephrosis
Distention dilation orf the renal pelvis and calices. Usually cause by urinary tract obstruction. Other casues can include retroperitoneal fibrosis and vesicoureteral reflux.
72
Renal cell carcinoma
Carcinoma of the proximal tubule cells. Clear cells with lipids/carbohydrates. Most common in 50-70 year old men.
Presents with hematuria, flank pain, and a palpable mass.
Can spread to renal vein and spread hematogenously after invasion of IVC. Will spread to lung and bone.
Associated with gene on chromosome 3. Associated with VHL. Causes a wide number of paraneoplastic syndromes like ACTH, epo, renin, pthrp. Treat with resection or immunotherapy.
Generally resistant to chemo and radiation.
73
Angiomyolipoma
Fatty kidney tumor seen in tuberous sclerosis.
74
Renal oncocytoma
Tumor of the epithelial lining of the collecting system. Well circumscribed benign mass that is composed of eosinophilic cells wihtout a perinuclearclearing. Painless hematuria, flank pain, and abdominal mass. Treat with nephrectomy.
75
Wilms tumor
most common renal malignancyof early childhood. Contains early glomerular like structures. Presents with a huge palpable flank mass +/- hematuria. Loss of function mutations inthe tumor suppresor genes WT1 or WT2 on chromosome 11. Can be part of beckwith wiederman syndrome (large tongue, organomegaly, muscular hemihypertrophy) or WAGR syndrome (wilms, aniridia, genitourinary malformation and mental retardation).
76
Transitional cell carcinoma
Often multifactorial and recur. Smoking is a big risk factor. Most common tumor of the urinarytract system. Can occur in calices pelvis ureters and bladder. Painless hematoria without casts. Can be caused by phenacetin, smoking, aniline dyes and cyclophosphamide.
Can be papillary or flat
Papillary starts as low, then high, then invades
Flat starts high, then invades. and is associated with early P53 mutations.
77
Squamous cell caricinoma of the bladder
Going to be seen in middle eastern young man with a schistosoma infection.
78
Adenocarcinoma of the bladder
Associated with urachal remnant at the doma of the bladder or glandular metaplasia.
79
Acute infectious cystitis
Inflammation of the urinary bladder that presents with pain nd dysturia. Systemic signs aregenerally absent (no fever, or chills) Risk factors include female gender, sex, and catheters.
Caused by e coli, staph sap, kleb, proteus, adenovirus
Positive for leuk esterase. Positive for nitrates if infection is with a gram negative organism.
Sterile pyuria suggests urethritis by n.gonorrheae or chlamydia.
80
Treat UTIs?
With fluoroquinolones or nitrofurantoin if pregnant.
81
Acute pyelonephritis
Affects cortex with relative sparing of glomeruli. Presents with dysuria fever and CVA tenderness. Most common cause is ascending UTI. Can also be caused by vesicoureteral reflux. Risk factors include Cath, obstruction, pregnancy, or diabetes.
82
Chronci pyelonephritis
Scarring with blunted calices and THYROIDIZATION OF KIDNEY (with eosinophilic casts). Caused by a malformation (like vesicoureteral reflux) or chronic kidney stones.
83
Drug induced interstitial nephritis
Acute interstitial renal inflammation. Pyria and azotemia especially with drugs like diuredics penicillins, sulfonamides, and rifampin. Can occur MONTHS after nsaids. Fever rash hematuria and CVA tenderness.
84
Diffuse cortical necrosis
Acute generalized cortical infarction of both kidneys usually due to a combination of vasospasm and DIC. Associated with abrutio placentae and septic shock.
85
ATN
Most common cause of intrinsic renal failure. Can be fatal. Death usuallyoccurs during oliguric phase. Key finding is granular casts in urine.
Caused by ischemia (hypotension, shock, sepsis, hemorrhage) or drugs (aminoglycosides, radioconstrast agents, lead, MYOGLOBINURIA, hemoglobinuria). Proximal tubule is most susceptible
86
Renal papillary necrosis
Sloughing of renal papillae can be associated with DM, sickle cell and chronic phenacitin use.
87
Acute kidney injury
Rapid decline in renal function with increases in creatinine and BUN over several days
88
Prerenal AKI
Due to hypotension usually. FENa 20. Urine osmolality is >500. Na and H2O and urea retained to save volume so BUN:CR goes up.
89
Renal AKI
Usually due to ATN. Backflow decreases GFR. Decrease in BUN:Cr due to less urea absorption. Urine NA/fena are both elevated.
90
Postrenal AKI
Caused by obstruction.
91
Symptoms of uremia
Increased bun and creatinine. Nausea and anorexia, pericarditis, asterixis, encephalopathy, platelet dysfunction (prevents aggregation and adhesion).
92
Renal osteodystrophy
Failure of vitamin D hydroxylation, hypocalcemia hyperphosphatemia, increase in pTH.
93
ADPKD
Cysts in enlarged kidneys, flank pain hematureia hTN chromosome 16. Or PKD2 on chromosome 4. Can cause berry aneurysms liver cysts
94
ARPKD
In kids, autosomal recessive, associated with hepatic fibrosis and portal hypertension. Significant renal failure.
95
Medullary cystic disease
Inherited disease causing tubulointerstitial fibrosis. Shrunken kidneys on ultrasound. can't concentrate urine
96
Simple vs complex cysts
Simple cysts are found in the outer cortex and are filled with ultrafilrate. Common. Complex cysts are septated require follow up. May predispose to renal cell carcinoma.
