Renal Flashcards
(499 cards)
1
Q
What is the peritoneal state of the kidneys?
A
Primary retroperitoneal (never had a mesentery)
2
Q
What is the peritoneal state of the ureter?
A
Primary retroperitoneal (never had a mesentery)
3
Q
The adrenal medulla is derived from…
A
Neural crest
4
Q
What vessels do the superior, middle, and inferior suprarenal arteries come off?
A
Superior - inferior phrenic artery; Middle - aorta artery; Inferior - Renal artery
5
Q
What vein does the right suprarenal vein drain into?
A
IVC
6
Q
What vein does the left suprarenal vein drain into?
A
L renal vein.
7
Q
The pronephros becomes…
A
Nothing (regresses)
8
Q
The mesonephros becomes…
A
Mesonephric (Wolffian) duct, which forms the ureteric bud, and becomes the male reproductive tract.
9
Q
The metanephros becomes..
A
The permanent kidney, ascending from the sacral region into the upper lumbar region.
10
Q
What (embryologically) forms the ureter?
A
The ureteric bud (from the caudal end of the mesonephros)
11
Q
What (embryologically) forms the nephrons of the adult kidney?
A
Metanephric mesoderm (up to DCT); Ureteric bud (collecting duct)
12
Q
What (embryologically) forms the urinary bladder?
A
The upper end of the urogenital sinus.
13
Q
The allantois becomes…
A
The urachus (a fibrous cord).
14
Q
The ureteric bud becomes…
A
The ureter, pelvis, calyces, and collecting ducts.
15
Q
What is Hartnup’s disease?
A
Deficiency in neutral amino acid (tryptophan) transporter. Results in pellagra (niacin deficiency).
16
Q
What artery does a horseshoe kidney get blocked by?
A
Inferior mesenteric a.
17
Q
What is the cause of death in Potter syndrome?
A
Lung hypoplasia
18
Q
What is Potter syndrome?
A
Oligohydramnios seen in bilateral renal agenesis or ARPKD. Results in: Lung hypoplasia (the cause of death in Potter syndrome); Flat face, low set ears, and extremity defects (result of compression of fetus due to oligohydramnios).
19
Q
What is multicystic dysplastic kidney?
A
A NON-INHERITED, congenital malformation of renal parenchyma characterized by cysts and abnormal tissue (e.g. cartilage). Be able to differentiate this from ARPKD.
20
Q
What will be seen in the liver in a patient with ARPKD?
A
Congenital hepatic fibrosis and hepatic cysts (think about this in a baby with portal HTN).
21
Q
What are some other disorders seen in patients with ADPKD?
A
Berry aneurysms, hepatic cysts, MVP.
22
Q
What is a major cause of sudden death in patients with ADPKD?
A
Rupture of berry aneurysms (SAH).
23
Q
What will be the gross appearance of the kidneys in a patient with medullary cystic kidney disease?
A
Shrunken kidneys (vs. enlarged cystic kidneys with ADPKD or ARPKD).
24
Q
What is the mechanism of inheritance of medullary cystic kidney disease?
A
AD
25
Where are the cysts located in medullary cystic kidney disease?
Medullary collecting ducts
26
What are the 3 subtypes of acute renal failure?
Prerenal, intrarenal, postrenal.
27
What is the BUN/Cr ratio in prerenal azotemia?
> 20
28
Why does the BUN/Cr ratio rise above 20 in prerenal azotemia?
Decreased blood flow to the kidney causes eventual release of aldosterone, which increases resorption of water. BUN is reabsorbed with water, raising the BUN in the blood. Creatinine is not reabsorbed, so the ratio increases.
29
What is the FENa in prerenal azotemia?
<1% (normal), because tubules are still intact and resorbing sodium well.
30
Why is the FENa <1% in prerenal azotemia?
Because the tubules are not damaged, so they are resorbing sodium regularly.
31
What will urine osmolality be in prerenal azotemia?
>500 (tubules can still concentrate urine well).
32
What causes postrenal azotemia?
Obstruction downstream from the kidney.
33
What increases the BUN/Cr ratio in early postrenal azotemia?
Back pressure forcing BUN back into the blood. Creatinine is NOT reabsorbed, so the ratio increases.
34
What is the BUN/Cr ratio in long-standing postrenal azotemia?
15 in early postrenal azotemia, but eventually, the tubules are damaged, resulting in decreased reabsorption of BUN and a decreased BUN/Cr ratio).
35
What is the BUN/Cr ratio in early postrenal azotemia?
>15 (back pressure forces BUN back into the blood. Creatinine is not reabsorbed, so the ratio increases).
36
What decreases the BUN/Cr ratio in long-standing postrenal azotemia?
Damage to the tubules with long standing postrenal azotemia results in impaired resorption of BUN, whose absorption was increased in early postrenal azotemia because of back pressure.
37
What is the FENAa in long standing postrenal azotemia?
>2%, because the tubules are damaged and sodium can't be effectively reabsorbed.
38
What will urine osmolality be in long standing postrenal azotemia?
t concentrate urine)
39
What is the most common cause of acute renal failure?
ATN (intrarenal azotemia)
40
What is the molecular cause of ATN?
Injury and necrosis of tubular epithelial cells plugs tubules, obstruction decreases GFR
41
What decreases the GFR in ATN?
Necrosis of cells plugging the tubules
42
What is seen in the urine in ATN?
Brown granular ("muddy") casts.
43
What is the BUN/Cr ratio in ATN (intrarenal azotemia)?
< 15 (damaged tubules, can't reabsorb BUN)
44
What is the FENa in ATN (intrarenal azotemia)?
>2% (damaged tubules, can't reabsorb sodium)
45
What is urine osmolality in ATN (intrarenal azotemia)?
t concentrate urine)
46
What are the two major etiologies of ATN?
Ischemia, nephrotoxins.
47
What part of the nephron is particularly susceptible to toxic ATN?
PCT (getting the highest concentration of drugs)
48
What two parts of the nephron are particularly susceptible to ischemic ATN?
PCT and TALOH
49
What antimicrobial family can cause ATN?
Aminoglycosides
50
What are some causes of toxic ATN?
Aminoglycosides, heavy metals, myoglobinuria, ethylene glycol, radiocontrast dye, urate (tumor lysis syndrome).
51
What is tumor lysis syndrome and what can be done to decrease the risk of it?
Rapid killing of leukemia cells causes release of purines, which are metabolized into uric acid, which can cause ATN. To decrease the risk, hydrate the patient well or give allopurinol.
52
What are the 3 phases of ATN?
1. Inciting event 2. Maintenance - oliguria (death most commonly occurs here!), risk of hyperkalemia. 3. Recovery phase - polyuric - BUN and Creatinine fall, risk of hypokalemia.
53
In which phase of ATN does death most commonly occur?
Oliguric (maintenance) phase due to hyperkalemia.
54
What is acute interstitial nephritis and what causes it?
Drug induced HSR of interstitium and tubules resulting in intrarenal ARF. Causes include NSAIDS, PCN, diuretics. Results in eosinophils in the urine. Resolves with cessation of drug, but can progress to renal papillary necrosis.
55
What will be seen on biopsy in acute interstitial nephritis?
Acute inflammatory infiltrate in CT between tubules. Tubules are spared.
56
What is seen in the urine in a patient with acute interstitial nephritis?
Eosinophils
57
Patient on NSAIDs presents with eosinophils in urine. Dx?
Acute interstitial nephritis (drug induced HSR to drug).
58
Chronic use of which two drugs can cause renal papillary necrosis?
Phenacetin, aspirin.
59
What are some causes of renal papillary necrosis?
Chronic analgesic abuse (phenacetin or aspirin), DM, sickle cell, pyelonephritis.
60
A patient abusing analgesics over a long period of time is at risk for which renal disorder?
Renal papillary necrosis.
61
What is the hallmark of nephrotic syndrome?
Proteinuria > 3.5 g/day
62
What happens to serum albumin in nephrotic syndrome?
Decreases (lost in protein - proteinuria >3.5 g/day), results in edema.
63
Why do patients with nephrotic syndrome become hypercoagulable?
Lose antithrombin III
64
What happens to cholesterol and lipid levels in a patient with nephrotic syndrome?
The patient becomes hypercholesterolemic and hyperlipidemic.
65
What is the most common cause of nephrotic syndrome in kids?
Minimal change disease
66
Minimal change disease is associated with what neoplasm?
Hodgkin's disease
67
What 3 things form the filtration barrier into the tubular space?
Endothelial cells, which sit on a basement membrane, which sits on podocytes (epithelial cells).
68
What is lost in minimal change disease?
Podocyte foot processes
69
What causes foot process effacement in minimal change disease?
Cytokines (which are massively overproduced in Hodgkin's disease, which is why patients with HL get MCD).
70
What is seen on H&E in minimal change disease?
Normal glomeruli
71
What is seen on EM in minimal change disease?
Effacement (flattening) of foot processes.
72
What protein is decreased in serum in minimal change disease?
Only albumin (not immunoglobulin).
73
What is the treatment for minimal change disease?
Corticosteroids (because damage is mediated by cytokines from T cells).
74
Does minimal change disease cause nephrotic or nephritic syndrome?
Nephrotic
75
Does focal segmental glomerulosclerosis cause nephrotic or nephritic syndrome?
Nephrotic
76
What is the most common cause of nephrotic syndrome in Hispanics and African Americans?
Focal segmental glomerulosclerosis (this is what Alonzo Mourning had)
77
A patient with sickle cell disease develops nephrotic syndrome. Dx?
Focal segmental glomerulosclerosis
78
A patient with HIV develops nephrotic syndrome. Dx?
Focal segmental glomerulosclerosis
79
A heroin addict develops nephrotic syndrome. Dx?
Focal segmental glomerulosclerosis
80
What is seen on H&E in focal segmental glomerulosclerosis?
Focal (not all glomeruli affected) and segmental (only part of the glomerulus affected) sclerosis (dark pink color).
81
A patient not responding to steroids in minimal change disease will progress to...
Focal segmental glomerulosclerosis
82
What will be seen on EM in focal segmental glomerulosclerosis?
Effacement of foot processes (just like MCD - patients who don't respond to steroids in MCD progress to FSGS).
83
Does membranous nephropathy give nephrotic or nephritic syndrome?
Nephrotic
84
What is the most common cause of nephrotic syndrome in Caucasian adults?
Membranous nephropathy
85
A patient with HBV develops nephrotic syndrome. Dx?
Membranous nephropathy most common, MPGN type I next most common.
86
A patient with SLE develops nephrotic syndrome. Dx?
Membranous nephropathy
87
A patient with HCV develops nephrotic syndrome. Dx?
Membranous nephropathy most common, type I MPGN next most common.
88
A patient with a solid cancer develops nephrotic syndrome. Dx?
Membranous nephropathy
89
What is seen on H&E in membranous nephropathy?
Thick glomerular basement membrane
90
What causes thickening of the basement membrane in membranous nephropathy?
Immune complex deposition
91
What is seen on EM in membranous nephropathy?
Subepithelial deposits with "spike and dome" appearance.
92
Subepithelial deposits with "spike and dome" appearance on EM
Membranous nephropathy (generate a "dome" of new BM over immune complex deposits with spikes between the domes).
93
What is seen on immunofluorescence in membranous nephropathy?
Granular appearance (due to immune complex deposition).
94
Anytime you see the word "membranous", in nephrotic syndrome, what is the underlying cause?
Immune complex deposition.
95
Does membranoproliferative glomerulonephritis cause nephrotic or nephritic syndrome?
Nephritic, nephrotic, or both
96
What causes the "tram track" appearance in membranoproliferative glomerulonephritis?
Mesangial cell proliferation cutting the glomerular BM in half, causing separation of the membrane.
97
Tram track appearance of GBM.
Membranoproliferative glomerulonephritis
98
What causes membranoproliferative glomerulonephritis?
Immune complex deposition
99
What is seen on immunofluorescence in membranoproliferative glomerulonephritis?
Granular appearance (immune complex deposition).
100
What are the two types of membranoproliferative glomerulonephritis?
Type I - subendothelial deposition, associated with HBV/HCV. Type II - intramembranous deposition, associated with C3 nephritic factor.
101
Where are the deposits in type I membranoproliferative glomerulonephritis?
Between the endothelium and the basement membrane (subendothelial).
102
Where are the deposits in type II membranoproliferative glomerulonephritis?
Within the basement membrane (intramembranous)
103
What infections are associated with type I membranoproliferative glomerulonephritis?
HBV/HCV
104
What is C3 nephritic factor?
Autoantibody that prevents the breakdown of C3 convertase, which drives complement, causing intramembranous immune depositions, which cause type II membranoproliferative glomerulonephritis.
105
C3 nephritic factor is associated with which disorder?
Type II membranoproliferative glomerulonephritis
106
Intramembranous complex deposits...
Type II membranoproliferative glomerulonephritis
107
Subendothelial complex deposits...
Type I membranoproliferative glomerulonephritis
108
Which subset of MPGN is more likely to cause the "tram track" appearance?
Type I (subendothelial depositions)
109
Diabetic nephropathy causes nephritic or nephrotic syndrome?
Nephrotic
110
What is the molecular etiology of diabetic nephropathy?
High serum glucose causing non-enzymatic glycosylation of vascular basement membranes resulting in hyaline arteriolosclerosis.
111
Which arteriole is preferentially damaged in diabetic nephropathy and what does damage of this arteriole cause?
Efferent arteriole damage (this is why ACE inhibitors are good in diabetics!!), causing backup of pressure in glomerulus and hyperfiltration, which leads to sclerosis of the mesangium of the glomerulus.
112
What is the first change in the kidney of a diabetic patient?
Non-enzymatic glycosylation of vascular basement membrane.
113
What is the hallmark of diabetic glomerulopathy?
Sclerosis of the mesangium and formation of Kimmelsteil-Wilson nodules
114
What are Kimmelsteil-Wilson nodules?
Dense nodular sclerosis of the mesangium seen in diabetic glomerulopathy.
115
Does systemic amyloidosis cause nephritic or nephrotic syndrome?
Nephrotic
116
How does amyloidosis cause nephrotic syndrome?
Deposits in the mesangium
117
Name the 6 glomerulopathies that cause nephrotic syndrome.
Minimal change disease; Focal segmental glomerulosclerosis; Diabetic glomerulopathy; Systemic amyloidosis; Membranous nephropathy; Membranoproliferative glomerulonephritis
118
What is the hallmark of nephritic syndrome?
Glomerular inflammation and bleeding
119
Quantify the proteinuria seen in nephritic syndrome.
<3.5 g/day
120
RBC casts are seen in nephrotic or nephritic syndrome?
Nephritic
121
What is the function of C5a?
Neutrophil chemotaxis
122
What virulence factor in strep pyogenes increases risk for PSGN?
M protein
123
How long after infection does PSGN occur?
2-3 weeks
124
Hypertension, salt retention, and periorbital edema are seen with nephritic or nephrotic syndrome?
Nephritic
125
What is seen on H&E in post-strep glomerulonephritis?
Hypercellular, inflamed glomerulus
126
What is seen on immunofluorescence in post-strep glomerulonephritis?
Granular appearance
127
What is seen on electron microscopy in post-strep glomerulonephritis?
Subepithelial "humps"
128
What is seen on H&E in rapidly progressive glomerulonephritis?
Crescents in Bowman's space
129
What composes the crescents seen in rapidly progressive glomerulonephritis?
Fibrin and macrophages
130
What is seen on immunofluorescence in Goodpasture's syndrome?
Linear immunofluorscence
131
Antibodies in Goodpasture's syndrome are targeted against...
Type IV collagen in glomerular (hematuria) and alveolar (hemoptysis) basement membranes
132
What is seen on immunofluorescence in diffuse proliferative glomerulonephritis?
Granular appearance
133
Where are the deposits seen in diffuse proliferative glomerulonephritis?
Subendothelial
134
What is the most common renal disease seen in SLE?
Diffuse proliferative glomerulonephritis
135
What is seen on renal immunofluorescence in Wegener's granulomatosis?
Nothing (pauci-immune)
136
What is seen on renal immunofluorescence in microscopic polyangiitis?
Nothing (pauci-immune)
137
What is seen on renal immunofluorescence in Churg-Strauss syndrome?
Nothing (pauci-immune)
138
List 3 causes of pauci-immune glomerulonephritis.
Churg-Strauss syndrome, microscopic polyangiitis, Wegener's granulomatosis. All are negative on immunofluorescence and should be worked up with an ANCA test.
139
Where does the p-ANCA antibody bind and which two causes of nephritic disease is it seen in?
Binds near the nucleus of the neutrophil (perineuclear). Seen in Microscopic polyangiitis and Churg-Strauss syndrome.
140
Where does the c -ANCA antibody bind and what nephritic disease is it seen in?
Binds in the cytoplasm of the neutrophil. Seen in Wegener's granulomatosis.
141
What 3 things bleed in Wegner's granulomatosis?
Nasal passages, lungs, kidneys (hematuria)
142
What 3 things are seen in Churg-Strauss syndrome that aren't seen in microscopic polyangiitis?
Granulomatous inflammation, Eosinophilia, Asthma (Both are p-ANCA positive)
143
What is seen on H&E in diffuse proliferative glomerulonephritis?
Wire looping of capillaries
144
What deposits in Berger disease, and where does it deposit?
IgA deposits (it is also called IgA nephropathy) in the mesangium of the glomeruli.
145
IgA nephropathy (Berger disease) typically follows...
A viral mucosal infection. End up producing excess IgA to fight the infection, which ends up depositing in the mesangium.
146
What is the common presentation and age group of IgA nephropathy (Berger disease)?
Episodic gross or microscopic hematuria with RBC casts usually following a mucosal infection. Seen in kids.
147
Production of what is decreased in Alport syndrome?
Type IV collagen
148
What is the method of transmission of Alport syndrome?
X-linked (85% dominant)
149
What happens to the basement membrane in Alport syndrome?
It is split due to a mutation in type IV collagen.
150
What are the 3 key findings in Alport syndrome?
Isolated hematuria, sensory hearing loss, visual disturbances.
151
Is Alport syndrome nephrotic or nephritic?
Nephritic.
152
List 6 causes of nephritic syndrome.
Acute post-streptococcal glomerulonephritis; Rapidly progressive glomerulonephritis (Wegener's, Goodpasture's, Microscopic polyangiitis, Churg-Strauss); Diffuse proliferative glomerulonephritis; Berger disease ( IgA nephropathy); Alport syndrome; Membranoproliferative glomerulonephritis
153
A patient with Henoch-Schoenlein purpura is at increased risk of developing what renal disorder?
IgA nephropathy (Berger disease)
154
What is seen on urine dipstick in cystitis?
Positive leukocyte esterase (due to leukocytes in urine); Nitrites (bacteria convert nitrates in urine into nitrites)
155
What is the #1 cause of cystitis?
E. coli
156
What is the #1 cause of cystitis in young sexually active women?
S. saprophyticus
157
Sterile pyuria is suggestive of...
Urethritis due to C. trachomatis or N. gonorrhoeae
158
What are the signs and symptoms of pyelonephritis?
Fever, flank pain, WBC casts, leukocytosis in addition to symptoms of cystitis (which has no systemic symptoms).
159
What is the #1 cause of acute pyelonephritis?
E. coli
160
Describe the appearance of the kidney in chronic pyelonephritis.
Cortical scarring with blunted calyces.
161
Scarring at the upper and lower poles of the kidneys is characteristic of...
Vesicoureteral reflux
162
What is "thyroidization" of the kidney and with what disease is it associated?
Plugging of the renal tubules with eosinophilic casts looks like thyroid tissue microscopically. This is seen in chronic pyelonephritis.
163
What type of renal stones are the most common?
Calcium stones (oxalate, phosphate)
164
What are the only renal stones that are radiolucent on x-ray?
Uric acid is radiolUscent
165
What causes ammonium magnesium phosphate stones?
Infection with proteus vulgaris or klebsiella species, which cause alkaline environment that leads to formation of the stone.
166
What type of renal stones are typically "staghorn"?
Ammonium magnesium phosphate stones ("struvite" or "triple")
167
Leukemia increases the risk for which type of renal stones?
Uric acid (due to increased cell turnover).
168
How are uric acid stones treated?
Alkalinization of urine (potassium bicarbonate) and hydration, allopurinol in patients with gout.
169
If you see a staghorn calculus in a child, what disorder should you think about?
Cystinuria (staghorne calculi are commonly cysteine in kids, struvite in adults).
170
How do you treat someone with cysteine stones?
Alkalinization of urine, hydration.
171
Why does renal failure cause anemia?
Reduced EPO
172
What cells in the kidney produce EPO?
Renal peritubular interstitial cells
173
Why do patients in renal failure develop hypocalcemia?
1. Can't excrete phosphate. Increased phosphate binds calcium in the blood. 2. Can't 1-alpha hydroxylate vitamin D (results in osteomalacia).
174
What is osteitis fibrosa cystica and why does it happen in renal failure?
High PTH due to hypocalcemia in renal failure causes resorption of calcium from the bone, which eventually causes fibrosis and cyst formation.
175
Patients on dialysis are at an increased risk for what cancer?
Renal cell carcinoma (secondary to shrunken kidneys that develop cysts in dialysis).
176
Tuberous sclerosis increases the risk for what renal neoplasm?
Angiomyolipoma (blood vessel, muscle, fat hamartoma)
177
Renal cell carcinoma arises from..
PCT cells
178
What is the triad of symptoms seen in renal cell carcinoma?
Hematuria, palpable mass, flank pain
179
List 4 potential paraneoplastic syndromes caused by renal cell carcinoma.
EPO - polycythemia; Renin - HTN; PTHrP - hypercalcemia; ACTH - Cushing syndrome
180
How does renal cell carcinoma cause a varicocele?
Invasion of the left renal vein blocks the L testicular vein
181
Explain the appearance of renal cell carcinoma on H&E.
Polygonal cells with clear cytoplasm - "clear cell".
182
Through which channels does renal cell carcinoma spread?
Veins
183
Pathogenesis of renal cell carcinoma involves loss of which tumor suppressor gene?
VHL (increases IGF-1 and HIF transcription factor which increases VEGF and PDGF).
184
How is Von Hippel-Lindau disease transmitted?
Autosomal dominant
185
Von Hippel-Lindau disease increases the risk for which two neoplasms?
Hemangioblastoma of the cerebellum and renal cell carcinoma.
186
What is the #1 renal tumor in children?
Wilms tumor
187
What is seen on biopsy of Wilms tumor?
Embryonic glomerular and tubular structures (blastema is the key component)
188
What is the classic presentation of Wilms tumor?
Large, unilateral flank mass with hematuria and hypertension (secondary to renin secretion).
189
What is the genetic component of Wilms tumor?
Deletion of tumor suppressor gene WT1 on chromosome 11. This is especially seen in WAGR syndrome and Beckwith-Widemann syndrome.
190
What is WAGR syndrome?
Wilms tumor; Aniridia; Genital anomalies; Developmental delay; seen with deletion of tumor suppressor gene WT1 on chromosone 11
191
What is Beckwith-Widemann Syndrome?
Wilms tumor; Neonatal hypoglycemia; Muscular hemyhypertrophy; Organomegaly (tongue); Seen with deletion of tumor suppressor gene WT1 on chromosome 11
192
What is the #1 risk factor for transitional cell carcinoma of the bladder?
Smoking (other risks are naphthylamine, azo dyes, and long term cyclophosphamide or phenacetin).
193
What is the general presentation of urothelial carcinoma?
Painless hematuria
194
What are the two pathways through which urothelial carcinoma can arise?
Flat - urothelial carcinoma that starts as high grade and invades. Associated with early p53 mutations. Papillary- starts as low grade, progresses to high grade, and invades.
195
p53 mutations are associated with what subtype of urothelial carcinoma?
Flat (starts as high grade, invades)
196
Schistosoma hematobium increases the risk for what cancer?
Squamous cell carcinoma of the bladder (boards will present this in a young, Middle-Eastern male with bladder CA)
197
In order to have squamous cell carcinoma of the bladder, there first must be...
Squamous cell metaplasia of the bladder
198
List 3 risk factors for squamous cell cancer of the bladder.
Chronic cystitis; S. hematobium; Long standing nephrolithiasis
199
Exstrophy of the bladder increases the risk for which type of cancer?
Adenocarcinoma of the bladder
200
Urachal remnant increases the risk for which type of cancer?
Adenocarcinoma of the dome of the bladder
201
What is the urachus and what is its function?
A tube that connects the fetal bladder to the yolk sac, allowing the bladder to drain in the yolk sac.
202
A patient presents with adenocarcinoma of the dome of the bladder (most superior portion). What most likely caused this?
Persistent urachus
203
What is cystitis glandularis and what does it increase the risk for?
Chronic inflammation of the bladder leading to columnar metaplasia, which can lead to adenocarcinoma of the bladder.
204
What is hydronephrosis?
Backup of urine into the kidney - can be caused by obstruction or vesicoureteral reflux and leads to parenchymal thinning in chronic cases.
205
What is the #1 risk factor in the oliguric (maintenance) phase of ATN?
Hyperkalemia
206
What is the #1 risk factor in the recovery phase of ATN?
Hypokalemia (patient is polyuric).
207
What is a renal oncocytoma?
Rare tumor that arises from collecting duct cells.
208
What serum protein will be reduced in patients with post-strep glomerulonephritis?
C3
209
What is the appearance of the glomerulus on H&E in a patient with post-strep GN?
Hypercellular with "lumpy bumpy" appearance.
210
What two things are deposited on the renal BM in Goodpasture syndrome?
C3 and IgG
211
What causes the cells to appear clear in renal cell carcinoma?
Glycogen and lipid accumulation
212
What three things are deposited on the BM in post-strep GN?
!gG, IgM, and C3.
213
What is the most important prognostic factor in patients with post-strep GN?
Age (kids much more likely to resolve)
214
What autoantibody is present in patients with idiopathic membranous glomerulopathy?
IgG to phospholipase A2 receptor (PLA2R)
215
What needs to be seen on urine culture in order to make a diagnosis of a UTI?
Greater than 100,000 colony forming units per mL
216
What does leukocyte esterase in a UTI mean?
UTI is bacterial
217
What do nitrites in urine mean in a UTI?
The bacteria is gram negative
218
What are the 3 drugs that can be given for acute, uncomplicated UTI?
TMP/SMX, nitrofurantoin, fosfomycin
219
What is the MOA of nitrofurantoin?
Reduced by bacterial flaviproteins to reactive intermediates, which inactivate many different bacterial processes.
220
Sulfamethoxazole inhibits...
Bacterial dihydropterate synthetase (Mimics PABA)
221
Trimethoprim inhibits...
Bacterial DHFR
222
What is the MOA of fosfomycin?
Inhibits production of murein monomers by binding to active site of cytoplasmic enolpyrivate transferase and preventing the addition of PEP to UDP-NAG (first step in cell wall synthesis).
223
What are the three first line drugs for acute pyelonephritis?
Ciprofloxacin, levofloxacin, TMP/SMX
224
In what patient group should asymptomatic bacteriuria be treated?
Pregnant women
225
Which UTI drugs are safe in pregnancy?
Fosfomycin, nitrofurantoin
226
TMP/SMX in pregnancy can have what effect on the fetus?
Kernicterus
227
What is the first line drug for acute pyelonephritis in a pregnant woman?
3rd generation beta lactam (ceftriaxone).
228
What does the sodium-cyanide/nitroprusside test test for?
Cystinuria - seen in young males with recurrent stones.
229
Hexagonal shaped crystals in urine
Cysteine stone
230
Envelope shaped crystals in urine
Calcium oxalate crystals - ethylene glycol poisoning.
231
WBC casts + symptoms of cystitis is pathogonomic for...
Acute pylelonephritis
232
What are the three embryological forms of the kidney?
Pronephros - Week 4 then degenerates
Mesonephros - interim kidney for first trimester, later contributes tot he male genital system
Metanephros - permanent - appears in 5th week of gestation
233
What is the ureteric bud?
Derived from caudal end of mesonephros; gives rise to ureter, pelvises, calyces, and collecting ducts
fully canalized by 10th week
Induces the metanephros to differentiate into the renal tubular epithelial structures
234
What is the Metanephric mesenchyme?
Ureteric bud induces this tissue to form the glomerulus through the distal convoluted tubules
235
What is the significance of the ureteropelvic junction?
Last to canalize - most common site of obstruction (hydronephrosis) in the fetus
236
What is the mnemonic for Potter's syndrome?
```
POTTER
Pulmonary hypoplasia (cause of death)
Oligohydraminos
Twisted skin (wrinkled)
Twisted face (facial deformities)
Extremities (limb deformities)
Renal agenesis
```
237
What type of infants commonly develop Potter's syndrome?
ARPKD, posterior urethral valves, bilateral renal agenesis
238
What part of the kidneys fuse in a horeshoe kidney?
Inferior poles of the kidneys
| note that the kidney functions normally
239
What type of patient do you often see with a horeshoe kidney?
Turner syndrome
240
What causes multicystic dysplastic kidney?
Abnormal interaction between the ureteric bud and metanephric mesenchyme
241
What are the findings in multicystic dysplastic kidney?
```
Leads to a nonfunctional kidney consisting of cysts and connective tissue.
If unilateral (most common) generally asymptomatic with compensatory hypertrophy of contralateral kidney
- often diagnosed prenatally via ultrasound
```
242
What are the 3 things that tell the juxtaglomerular cells to release renin?
1. beta-1 adrenergic stimuli (increased sympathetics)
2. Low sodium in the distal convoluted tubule (sensed via macula densa)
3. Low pressure in afferent arterioles of glomerulus
243
What is the function of the juxtaglomerular cells? of the macula densa?
Juxtaglomerular cells: secrete renin and monitor BP
| Macula densa cells: senses sodium levels
244
Which part of the kidney contains the glomeruli and which part contains the nephrons?
Cortex contains the glomeruli
| Medulla contains the nephrons
245
What is the significance of the location of the ureters and arteries?
Ureters pass under the uterine artery and under the ductus deferens (retroperitoneal)
246
How much of the total body weight is total body water?
60%
247
How much of the total body water is:
- extracellular fluid
- intracellular fluid
- plasma volume
- interstitial volume
Total body water is 60% of total body weight
Extracellular fluid is 1/3 of total body water
intracellular fluid is 2/3 of total body water
plasma volume is 1/4 of extracellular fluid
interstitial volume is 3/4 of extracellular fluid
248
What is the 60 - 40 -20 rule?
60% total body water
40% ICF
20% ECF
249
How is plasma volume measured?
by radiolabeled albumin
250
How is extracellular volume measured?
by inulin
251
What 3 things make of the glomerular filtration barrier?
1. fenestrated capillary endothelium (size barrier)
2. Fused basement membrane with heparin sulfate (negative charge barrier)
3. Epithelial layer consisting of podocyte foot processes
252
What happens with a loss of the charge barrier in the glomerular filtration barrier?
The charge barrier is lost in nephrotic syndrome which leads to albuminuria. hypoproteinemia, generalized edema and hyperlipidemia
253
What is the formula for renal clearance?
```
Clearance = (Urine concentration x urine flow rate) / Plasma concentration
C = UV/P
```
254
What are the there possibilities with Renal clearance?
Cx < GFR = net tubular reabsorption of x
Cx > GFR = net tubular secretion of x
Cx = GFR = no net secretion or reabsorption (ie inulin)
255
What can be used to calculate GFR?
Inulin can be used to calculate GFR because it is freely filtered and is neither reabsorped nor secreted
256
What is the formula for GFR?
GFR = Uinulin x V / Pinulin = Cinulin
Note that creatinine clearance is an approximate measure of GFR - slightly overestimates GFR because it's moderately secreted by renal tubules
257
What is the oncotic pressure in bowman's space normally?
0
258
What is normal GFR?
~100 mL/min
259
What is the formula for effective renal plasma flow?
Renal plasma flow = PAH clearance = Urine PAH x V/ P PAH
260
What can be used to measure the effective renal plasma flow?
The clearance of PAH (para-amino hippuric acid) which is both filtered and actively secreted into the proximal tubule
261
What is the formula for renal blood flow?
RBF = RPF/(1-hematocrit)
262
What is the formula for filtration fraction?
Filtration Fraction = GFR of inulin / RPF of PAH
Filtration fraction is the portion of blood going to the kidney that's filtered through the glomerulus
263
What does dehydration cause?
way decreased renal plasma flow
decreased GFR
increased filtration fraction
264
What is a normal filtration fraction?
20%
265
What is a filtered load equation?
Filtered load = GFR x plasma concentration
266
What effect do prostaglandins have on the afferent arteriole?
Prostaglandins dilate the afferent arteriole leading to increased RPF and increased GFR and a constant FF
note that NSAIDS will cause the exact opposite since they inhibit prostaglandins, they will lead to constriction at the afferent arteriole
267
What effect does Angiotensin II have on the efferent arteriole?
Angiotensin II preferentially constricts the efferent arteriole leading to decreased RPF, increased GFR and therefore increased FF
Note that ACE inhibitors block angiotensin II and therefore will dilate the efferent arteriole having the opposite effect
268
What are glomerular dynamics that will be seen with afferent arteriole constriction?
decreased RPF
decreased GFR
no change to FF
269
What are glomerular dynamics that will be seen with Efferent arteriole constriction?
Decreased RPF
Increased GFR
Increased FF
270
What are glomerular dynamics that will be seen with Increased plasma protein concentration?
No change in RPF
Decreased GFR
Decreased FF
Note that with increased serum protein you have increased osmotic pull so less blood will escape
271
What are glomerular dynamics that will be seen with Decreased plasma protein concentration?
No change in RPF
Increased in GFR
Increased in FF
272
What are glomerular dynamics that will be seen with constriction of the ureter?
No change in renal plasma flow
decreased GFR
decreased FF
273
What are glomerular dynamics that will be seen with dilation of the afferent arteriole?
Increased RPF
Increased GFR
constant FF
274
What is the formula for excretion rate?
U[x] x V = urinary concentration of x times the urine flow rate
275
What is the formula for reabsorption?
Reabsorption = Filtered - excreted
276
What is the formula for secretion?
Secretion = excreted - filtered
277
What is normal glucose clearance?
Glucose at a normal plasma level is completely reabsorbed in the proximal tubule by Na+/glucose cotransport
278
When do you start to see glucose in the urine?
At plasma glucose of ~ 160mg/dl, glucosuria begins (threshold)
At 350 mg/dL all transporters are full saturated (Tm)
279
What happens in pregnancy with glucose and amino acids?
Normal pregnancy reduces reabsorption of glucose and amino acids in the proximal tubule leading to glucosuria and aminoaciduria
280
What is Hartnup's disease?
Deficiency of neutral aminoa acid (tryptophan) transporter - results in pellagra
No tryptophan = no niacin (Vit B3) = 3 D's of pellagra = Dermatitis, diarrhea, dementia and maybe death
281
Which part of the kidney uses isotonic absorpotion?
Early proximal tubule
282
What does PTH do in the proximal tubule?
Inhibits Na/phosphate co transport leading to phosphate excretion
283
What does Angiotensin II do in the proximal tubule?
Stimulates Na/H exchanger leading to increased sodium, water and bicarb reabsorption
This permits a contraction alkalosis
284
What is the concentrating segment of the nephron?
Thin descending loop of henle
| Makes urine hypertonic
285
What solute is impermeable in the thin descending loop of henle?
Sodium!
| The thin descending loop passively reabsorbs water via medullary hypertonicity and it is impermeable to sodium
286
What portion of the kidney actively reabsorbs sodium, potassium and chloride?
Thick ascending loop of henle.
Indirectly induces the paracellular reabsorption of magnesium and calcium through positive lumen potential generated by potassium back lead
287
What section of the nephron is impermeable to water?
Thick ascending loop of Henle.
| This section makes the urine less concentrated as it ascends
288
What portion of the nephron actively reabsorbs sodium and chloride and makes the urine hypotonic?
Early distal convoluted tubule
289
What effect does PTH have at the early distal convoluted tubule?
Increased calcium/sodium exchange leading to increased calcium reabsorption
290
What portion of the nephron is regulated by aldosterone and what are the effects?
Collecting tubules
aldosterone reabsorbs sodium in exchange for secreting potassium and hydrogen
- Aldosteron acts on mineralocorticoid receptor leading to the insertion of sodium channels on the luminal side
291
Where in the nephron does ADH have it's effect and what does it do?
ADH works at the collecting tubule principal cell at the V2 receptor causing insertion of aquaporin water channels on the luminal side
292
Why does tubular inulin increase in concentration (but not amount) along the proximal tubule?
As a result of water reabsorption
| and inulin is neither reabsorbed or secreted
293
What is the function of Angiotensin II on the vascular smooth muscle?
Angiotensin II acts at AT1 receptors on the vascular smooth muscle to cause vasoconstriction and an increased in BP
294
What is the function of Angiotensin II on the efferent arteriole off the glomerulus?
Angiotensin II causes constriction of the efferent arteriole of the glomerulus leading to increased filtration fraction to preserve renal function (GFR) in low-volume states (like when RBF is decreased)
295
What is the function of Angiotensin II on The adrenal gland?
Angiotensin II causes release of aldosterone.
- Aldosterone increased sodium channel and Na/K pump insertion in principal cells in the kidney
- This enhances K+ and H+ excretion (upregulates principal cell K+ channels and intercalated cell H+ channels)
- This creates favorable Na+ gradient for Na and water reabsorption
296
What is the function of Angiotensin II on the posterior pituitary?
Angiotensin II functions to increase ADH release from the posterior pituitary resulting in increased water channel insertion in principal cells leading to increased water reabsorption
297
What is the function of Angiotensin II on the proximal tubule?
Angiotensin II increased proximal tubule Na/H activity leading to sodium, bicarb, and water reabsorption (permits contraction alkalosis)
298
What is the function of Angiotensin II on the hypothalamus?
Stimulates hypothalamus leading to increased thirst
299
What is the function of Angiotensin II on baroreceptors?
Angiotensin II affects baroreceptors function by limiting reflex bradycardia which would normally accompany it's pressor effects - helps to maintain blood volume and blood pressure
300
What is the function of ANP?
Released from the atria in response to increased volume
- may act as a "check" on the R-A-A system
- relaxes vascular smooth muscle via cGMP causing increased GFRP and decreased renin
301
What is the function of ADH?
Primarily regulates osmolarity but also responds to low blood volume, which takes precedence over osmolarity
302
What is the function of Aldosterone?
Primarily regulates blood volume, in low volume states both ADH and aldosterone act to protect blood volume
303
What comprises the juxtaglomerular apparatus?
- JG cells (modified smooth muscle of afferent arteriole)
| - macula densa (NaCl sensor, part of the distal convoluted tubule
304
Can beta blockers decrease renin release?
Beta blockers can decrease BP by inhibits Beta 1 receptors of the JGA causing decreased renin release
305
What is Erythropoietin?
released by interstitial cells in the peritubular capillary bed in response to hypoxia
306
How does the kidney increase vitamin D levels?
PTH acts on the kidney to increase 1 alpha hydroxylase in the kidney which causes the proximal tubule cells to convert 25-OH vitamin D to 1,25 OH2 vitamin D (active form)
307
What is the kidney endocrine function with prostaglandin?
Paracrine secretion vasodilates the afferent arterioles to increase GFR
308
What can NSAIDS cause in the kidney?
NSAIDS can cause acute renal failure by inhibiting the renal production of prostaglandins, which keep the afferent arterioles vasodilated to maintain GFR
309
What is the effect of ANP on the nephron?
Causes increased GFR and increased sodium filtration at the proximal tubule with no compensatory sodium reabsorption in the distal nephron
Net effect is sodium loss and volume loss
310
List 6 things that cause a shift of potassium out of the cell causing hyperkalemia
1. Digitalis
2. Hyperosmolarity
3. insulin deficiency (ie diabetic ketoacidosis)
4. lysis of cells
5. Acidosis (via H/K pump)
6. Beta adrenergic antagnosits
311
Lost three things that can treat hyperkalemia
Albuterol
Insulin (give dextrose first!)
Bicarb
312
List 4 things that shifts potassium into the cells causing hypokalemia
1. Hypo-osmolarity
2. insulin (increased Na/K ATPase)
3. Alkalosis
4. Beta adrenergic agonist (increased Na/K ATPase)
313
Compare what happens with low and high serum sodium levels?
Low - nausea and malaise, stupor and coma
High - irritability, stupor, coma
314
Compare what happens with low and high serum Potassium levels?
Low - U waves on ECG, flattened T waves, arrhythmias, muscle weakness
High - Wide QRS and peaked T waves on ECG, arrhythmias and muscle weakness
Remember that T waves mirror K+ levels
315
Compare what happens with low and high serum calcium levels?
Low - tetany, seizures, positieve trousseau sign, Chvostek sign
High - Stones (renal), bones (pain), groans (abdominal pain), psychiatric overtones (anxiety, altered mental status), but not nevessarily calciuria
Remember, decreased extracellular calcium leads to INCREASED membrane excitability
316
Compare what happens with low and high serum Magnesium levels?
Low - tetany, arrhythmias can lead to torsades de pointes
High - decreased deep tendon reflexes, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia
317
Compare what happens with low and high serum phosphate levels?
Low - Bone loss and osteomalacia
High - Renal stones, metastatic calcifications, hypocalcemia
318
What should be seen with a compensatory mechanism in a acid-base disturbance?
A compensatory mechanism should never bring the pH all the way back into the normal rage.
If it's normal and PCO2 and bicarb are both wacked then most likely its a mixed situation.
319
What is the Winter's formula?
PCO2 = 1.5 (bicarb) + 8 plus or minus 2
320
When is the Winter's formula used?
Winter's formular predicts the respiratory compensation for a simple metabolic acidosis
PCO2 = 1.5 (bicarb) + 8 plus or minus 2
If the measured PCO2 differs significantly from the predicted PCO2, then a mixed acid-base disorder is likely present
321
What 6 things cause hypernatremia?
```
6 Ds:
Diuretics
Dehyrdation
Diabetes insipidus
Docs (iatrogenic)
Diarrhea
Diseases of the kidney
```
322
What can cause a high anion gap metabolic acidosis?
```
MUDPILES
Methanol (formic acid)
Uremia
Diabetic ketoacidosis
Propylene glycol
Iron tables or INH
Lactic acidosis
Ethylene glycol (oxalic acid)
Salicylates (late)
```
323
How do you measure anion gap?
anion gap = Na - (Cl + biacrb)
normal anion gap = 8-12
324
What can cause a normal anion gap metabolic acidosis?
```
HARD-ASS
Hyperalimentation
Addison's disease
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
```
325
What can cause a respiratory acidosis?
Hypoventilation
- airway obstruction
- acute lung disease
- chronic lung disease
- opioids, sedatives
- weakening of respiratory muscles
326
What can cause a respiratory alkalosis?
Hyperventilation
- early high altitude exposure
- Salicylates (early)
- anxiety, panic attack
- acute hypoxemia (PE)
327
What can cause a metabolic alkalaosis?
- loop diuretics
- vomiting
- antacid use
- Hyperaldosteronism
328
Describe Type 1 Renal tubular acidosis
This is "distal"
Impaired Hydrogen excretion "H" = one letter (type I)
- Defect in collecting tubule's ability to excrete H
Untreated patients have a urine pH >5.5
associated with hypokalemia.
Increase risk for calcium phosphate stones as a result of increased urine pH and bone resorption
329
What are patients with Type 1 Renal tubular acidosis at increased risk for?
Calcium phosphate kidney stones as a result of increased urine pH and bone resorption
330
Describe Type 2 renal tubular acidosis
"proximal"
Defect in proximal tubule bicarb reabsorption.
May be seen with fanconi's syndrome
Uncreated patients typically have a urine pH <5.5 associated with hypokalemia
Increased risk for hypophosphatemic rickets
331
What are patients with type 2 renal tubular acidosis at increased risk for?
Increased risk for hypophosphatemic rickets
332
Describe Type 4 renal tubular acidosis
"Hyperkalemic"
Hypoaldosteronism or lack of collecting tubule response to aldosterone.
The resulting hyperkalemia impairs ammoniagenesis in the proximal tubule leading to decreased buffering capacity and decreased urine pH
Can't generate NH4+
333
What is the mnemonic for remembering the defect with Type 4 renal tubular acidosis?
Impaired ammonium excertion
| "NH4" (4) or low ALDOsterone (4 letters)
334
What is the defect in type 2 renal tubular acidosis similar to?
Similar to the effects of Acetazolamide
335
What is seen with bladder cancer and kidney stones?
Hematuria with no casts
336
What is seen in acute cystitis?
pyuria with no casts
337
What do seeing casts in the urine mean?
Presence of casts indicates that hematuria/pyuria is of renal (vs blader) origin
338
With what conditions would you see RBC casts?
Glomerulonephritis, ischemia, or malignant hypertension
339
With what conditions would you see WBC casts?
Tubulointerstitial inflammation, acute pyelonephritis, transplant rejection
340
With what conditions would you see Fatty casts ("oval fat bodies")?
Nephrotic syndrome
341
With what conditions would you see granular ("muddy brown") casts?
Acute tubular necrosis
342
With what conditions would you see waxy casts?
Advanced renal disease/chronic renal failure
note that the most common cause of chronic renal failure is poorly controlled diabetes
343
With what conditions would you see Hyaline casts?
Nonspecific, can be a normal finding
Hyaline casts are solidified Tamm-Horsfall protein secreted from tubular epithelial cells
344
Which two kidney diseases can be seen as both Nephritic and Nephrotic syndromes?
Diffuse proliferative glomerulonephritis
| Membranoproliferative glomerulonephritis
345
Why do you see lipiduria/oval fat bodies in nephrotic syndrome?
You have massive proteinuria resulting in decreased plasma proteins which leads to edema
Because you depleted the serum albumin and lose the colloid oncotic pressure, the liver tries to compensate by generating lipids in an attempt to maintain osmotic pressure gradient
346
Describe the findings in a patient with Nephrotic syndrome
A patient presents with massive proteinuria (>3.5 g/day) and frothy urine. They have hyperlipidemia, fatty casts and edema.
They also have thromboembolism due to a loss of ATIII in the urine
and increased risk of infections due to loss of immunoglobulin in the urine
347
Why are patients with nephrotic syndrome hypercoagulable?
They have a lost of AT III in their urine making them have thromboembolisms
348
Why do patients with nephrotic syndrome have an increased risk of infection?
Immunoglobulinuria
349
A patient presents with massive proteinuria (>3.5 g/day) and frothy urine. They have hyperlipidemia, fatty casts and edema.
Nephrotic syndrome
350
Light microscopy shows segmental sclerosis and hyalinosis - what will you see on EM?
This is focal segmental glomerulosclerosis
| EM will show effacement of foot processes similar to minimal change disease
351
What is the most common cause of nephrotic syndrome in adults?
Focal segmental glomerulosclerosis
352
What is the most common cause of nephrotic syndrome in latinos and African americans?
Focal segmental glomerulosclerosis
353
What 5 things are associated with focal segmental glomerulosclerosis?
```
HIV infection
Heroin abuse
Massive obesity
interferon treatment
chronic kidney disease due to congenital absence or surgical removal
```
354
Light microscopy shows diffuse capillary and diffuse glomerular basement thickening, what will you see on EM?
This is membranous nephropathy
| EM will show spike and dome appearance with subepithelial deposits
355
What is seen on immunofluorescence in Membranous nephropathy?
Granular
356
What is the second most common cause of primary nephrotic syndrome in adults?
Membranous nephropathy
357
What is the nephropathy presentation of an SLE patient?
Membranous nephropathy
358
What is deposited and where in a patient with membranous nephropathy?
Subepithelial deposits of IgG, C3, K and lambda light chains
note that the mesangium is normal
359
A patient presents with normal glomeruli on light microscopy, what will be seen on EM?
This is minimal change disease (lipoid nephrosis)
EM will show foot process efacement
360
What is lost in a patient with minimal change disease?
Selective loss of albumin but not globulins
| caused by GBM polyanion loss
361
A patient presents with a recent infection or immunization - what nephropathy are they at risk of getting?
Minimal change disease
Most common in children.
responds well to corticosteroids
362
A patient presents with congo red stain showing birefringence under polarized light due to mesangial deposits of what?
This is amyloidosis causing a nephrotic syndrome
363
What can cause amyloidosis nephropathy?
A chronic condition like multiple myeloma, TB or rheumatoid arthritis
364
Describe the differences between Type I and Type II membranoproliferative glomerulonephritis
Type 1 - subendothelial immune complex deposits with granular immunofluorescence. Shows "tram track" appearance due to GBM splitting caused by mesangial ingrowth
Type II - Intramembranous immune complex deposits
365
What is type 1 membranoproliferative glomerulonephritis associated with?
HBV and HCV
366
What is type 2 membranoproliferative glomerulonephritis associated with?
C3 nephritic factor
367
Proliferation of mesangial and endothelial cells of the glomeruli and expansion of the mesangial matrix along with immune deposits
membranoproliferative glomerulonephritis
368
What occurs in diabetic glomerulonephropathy?
Nonenzymatic glycosylation of the glomerular basement membrane leading to increased permeability and thickening
369
What occurs in diabetic glomerulonephropathy at the efferent arterioles?
Nonenzymatic glycosylation of the efferent arteriole leads to increased GFR and then to mesangial expansion
370
What is seen on light microscopy with a patient with diabetic glomerulonephropathy?
- Mesangial expansion, glomerular basement membrane thickening
- eosinophilic nodular glomerulosclerosis = Kimmelstiel-Wilson nodules
371
Describe the common presentation seen in nephritic syndrome
Inflammatory process
When it involves the glomeruli, it leads to hematuria and RBC casts in the urine. Associated with azotemia, oliguria, hypertension and proteinuria (<3.5 g/day)
372
A patient presents with inflammation and hematuria and RBC casts in the urine. Associated with azotemia, oliguria, hypertension and proteinuria (<3.5 g/day)
Nephritic syndrome
373
What type of hypersensitivity is acute postsreptococcal glomerulonephritis?
Type III HS
| Immune complexes get deposits in the glomeruli
374
A patient presents with glomeruli enlarged and hypercellular, neutrophils within the glomerulus and a "lumpy bumpy" appearance - what would be seen on EM?
This is acute poststreptococcal glomerulonephritis
| EM would show subepithelial immune complex humps
375
What does the IF show in poststreptoccocal glomerulonephritis?
granular appearance due to IgG, IgM and C3 deposition along the GBM and mesangium
376
What is the clinical findings in a patient with poststreptococcal glomerulonephritis? What test should you do?
Most frequently seen in children.
Peripheral and periborbital edema, dark urine (Coca-Cola colored) and hypertension.
Resolves spontaneously
An anti-streptolysin O titer would confirm diagnosis
377
A patient gets a group A beta hemolytic strep infection - giving them antibiotics will protect them against what?
Rheumatic fever and rheumatic heart disease
| but it will NOT protect against poststreptococcal glomerulonephritis
378
Light microscopy shows crescent moon shapes within a glomerulus and the patient has rapidly deteriorating renal function - what is contained within the crescents and what is the diagnosis?
Rapidly progressive (crescentic) glomerulonephritis
The crescents consist of fibrin and plasma proteins with glomerular parietal cells, monocytes, and macrophages
379
List three diseases that can present with Rapidly progressive (crescentic) glomerulonephritis?
- Goodpasture's syndrome - type II HS with antibodies tot GBM and alveolar basement membrane giving a linear IF
- Granulomatosis with polyangiitis (Wegener's) - c-ANCA +
- Microscopic polyangiitis - p-ANCA +
380
What is the most common cause of death in SLE patients?
Diffuse proliferative glomerulonephritis
381
List two things that can cause Diffuse proliferative glomerulonephritis?
1. SLE
| 2. Membranoproliferative glomerulonephritis
382
Light microscopy shows wire looping of capillaries - what will be seen on EM and IF?
This is diffuse proliferative glomerulonephritis
EM will show subendothelial and sometimes intramembranous IgG based immune complexes often with C3 deposition
IF will be granular
383
A patient has Henoch-Schonlein purpura, what nephritic syndrome are they most likely to get?
Berger's disease (IgA nephropathy)
384
What will be seen in LM, EM and IF in a patient with Berger's disease?
LM - Mesangial proliferation
EM - Mesangial immune complex deposits
IF - IgA based immune complex deposits in the mesangium
385
What is the tetrad seen in Berger's disease?
palpable purpura on the butts and legs
arthralgias
abdominal pain
renal disease
386
What causes Berger's disease?
Often presents/flares with a URI or acute gastroenteritis
387
A patient presents with glomerulonephritis, deafness and eye problems - what is the diagnosis?
Alports syndrome (AKA hereditary nephritis)
388
What is the defect in Alports syndrome - and what does it cause in the kidney?
Mutation in type IV collagen leading to split basement membrane
X-linked
389
What is the outcome of a patient with rapidly progressive crescentic glomerulonephritis?
poor prognosis, rapidly deteriorating renal function (days to weeks)
390
What is the most common type of kidney stone?
Calcium oxalate
391
What causes precipitation of calcium oxalate stone?
decreased pH
392
What causes precipitation of calcium phosphate stone?
increased pH
393
Which stone is radiolucent on Xray?
Uric acid stone
394
What can cause calcium oxalate stones?
oxalate crystals can result from ethylene glycol (antifreeze) or vitamin C abuse
395
What is the treatment for calcium kidney stones?
thiazides and citrate for recurrent stones
396
What is the most common kidney stone presentation?
calcium oxalate stone in a patient with hypercalciuria and normocalcemia
397
what can generally cause calcium stones if a patient hasn't ingested anything bad..?
conditions that cause hypercalcemia (cancers, increased PTH), things that can increase calciuria
398
What pH do ammonium magnesium phosphate stones precipitate at?
increased pH
399
What causes ammonium magnesium phosphate stones?
caused by infection with urease-positive bugs like proteus mirabilis, staphylococcus and klebsiella
They hydrolyze urea to ammonia leading to urine alkalinization
400
What is a common cause of staghorn calculi?
ammonium magnesium phosphate (struvite) stones
401
Uric stones are radiolucent on Xray - is there another way to see them?
they are visible on CT and ultrasound
402
When do you see uric acid stones?
- stone association with hyperuricemia ( gout)
| - often seen in diseases with increased cell turnover like leukemia
403
At what urine pH do you see uric acid stones?
decreased pH
404
What is the treatment of uric acid stones?
alkalinization of the urine
405
At what pH do you see cystine stones?
Precipitates at decreased pH
| causes hexagonal crystals
406
What causes cystine stones?
most often secondary to cystinuria.
407
How do you treat cystine stones?
Alkalinization of the urine
408
A 36 yo F has kidney stones and she gets pain in her right flank to her groin - what is a muscle that's being affected as part of a viscerosomatic response?
psoas MAJOR
409
Describe hydronephrosis
Backup of urine into the kidney.
Can be cuased by urinary tract obstruction or vescoureteral reflux.
causes dilation of renal pelvis and calyces proximal to obstruction.
May result in parenchymal thinning in chronic severe cases
410
what cells to renal cell carcinoma originate from?
Originates from proximal tubule cells
| this is why they are polygonal clear cells filled with accumulated lipids and carbohydrates
411
how does renal cell carcinoma manifest clinically?
Hematuria, palpable mass, secondary polycythemia (XS EPO), flank pain fever and weight loss
412
Who gets renal cell carcinoma?
Most common in men 50-70 yo with increased incidence with smoking and obesity
413
Where does renal cell carcinoma spread to?
It invades the renal vein then the IVC and spreads hematogenously
Metastasizes to lung and bone
414
How do you treat renal cell carcinoma/
resection is it's localized
| it's resistant to conventional chemotherapy and radiation therapy
415
what gene deletion is renal cell carcinoma associated with?
gene deletion on chromosome 3 (deletion may be sporadic or inherited as von hippel-lindau syndrome)
416
What can cause a nephroblastoma?
This is a Wilms' tumor
deletion of tumor suppressor gene WT1 on chromosome 11
May be part of Beckwith-Wiedemann syndrome or WAGR complex
417
What is the most common renal malignancy of early childhood (2-4 yo)?
Wilm's tumor (nephroblastoma)
418
How does a nephroblastoma present?
huge palpable flank mass and/or hematuria in a 2-4 yo
note that it will contain embryonic glomerular structures
419
What is the most common tumor of the urinary tract system and where can it occur?
Transitional cell carcinoma
can occur in renal calyces, renal pelvis, ureters, and bladder
420
What suggest bladder cancer?
Painless hematuria (no casts!)
421
What can cause transitional cell carcinoma?
```
Associated with problems in your P SAC
Phenacetin
Smoking
Aniline dyes
Cyclophosphamide
```
422
A patient presents with fever, costovertebral angle tenderness, nausea and vomiting with white cell casts in the urine - what's happening?
Acute pyelonephritis
affects the cortex with relative sparing of the glomeruli/vessels
423
What causes coarse, asymmetric corticomedulalry scarring with blunted calyces and tubules that contain eosinophilic casts?
Chronic pyelonephritis
thyroidization of the kidney!
424
What causes chronic pyelonephritis?
recurrent episodes of acute pyelonephritis
| typically requires predisposition to infection like vescoureteral reflux or chronically obstruction kidney stones
425
What causes drug induced interstitial nephritis?
AKA tubulointerstitial nephritis
drugs that act as haptens, inducing hypersensitivity
nephritis typically occurs 1-2 weeks after certain drugs are given but can occur months after starting NSAIDS
426
What drugs can cause drug induced interstitial nephritis?
diuretics, penicillin derivatives, sulfonamides, rifampin and NSAIDs
427
what is the clinical findings in drug induced interstitial nephritis?
associated with fever, rash, hematuria, and costovertebral angle tenderness or it can be asymptomatic.
often see pyuria (classically eosinophils) and azotemia
428
What is diffuse cortical necrosis?
Acute generalized cortical infarction of BOTH kidneys likely due to a combination of vasospasm and DIC
429
What is diffuse cortical necrosis associated with?
Associated with obstetric catastrophes and septic shock
430
What is the key finding in a patient with acute tubular necrosis?
granular muddy brown casts
431
What is the most common cause of intrinsic renal failure?
Acute tubular necrosis
432
What is the result in someone with acute tubular necrosis?
It's self reversible in some cases but can be fatal if left untreated
death most often occurs during the initial oliguric phase
433
List the 3 stages of acute tubular necrosis
1. inciting event
2. maintenance phase - oliguric; lasts 1-3 weeks; risk of hyperkalemia
3. Recovery phase - polyuric; BUN and serum creatinine fall; risk of hypokalemia
434
What is acute tubular necrosis associated with?
renal ischemia like shock and sepsis, crush injury (myoglobinuria), drugs and toxins
435
Describe renal papillary necrosis
Sloughing of renal papillae leading o gross hematuria and proteinuria. May be triggered by a recent infection or immune stimulus
436
What is renal papillary necrosis associated with?
Diabetes mellitus
Acute pyelonephritis
Chronic phenacetin use (acetaminophen is phenacetin derivative)
Sickle cell anemia and trait
437
how is acute renal failure defined?
abrupt decline in renal function with increased creatinine and increased BUN over a period of several days
438
Describe prerenal azotemia?
As a result of decreased RBF leading to decreased GFR
| sodium and water and urea are retained by the kidney in an attempt to conserve volume so BUN/Cr ratio increase
439
List 4 things that can cause pre-renal azotemia
Hypovolemia
Shock
hypotension
renal vasoconstriction with NSAIDs
440
Describe intrinsic renal failure
generally due to acute tubular necrosis or ischemia/toxins; less commonly due to acute glomerulonephritis.
Patchy necrosis leads to debris obstructing the tubule and fluid backflow across the necrotic tubule
- decreased GFR
- urine has epithelial/granular casts
-Buns reabsorption is impaired leading to decreased BUN/Cr ratio
441
List 5 things that can cause intrinsic renal failure
```
Acute interstitial necrosis
glomerulonephritis
acute tubular necrosis
DIC
acute pyeonephritis
```
442
Describe postrenal azotemia
Due to outflow obstruction. develops only with BILATERAL obstruction
443
List 4 things that can cause postrenal azotemia
Stones
BPH
neoplasia
congenital anomalies
444
Describe the urine osmolarity, urine sodium, FENA, and serum BUN/Cr seen in prerenal azotemia?
Urine osmolarity: >500
Urine sodium: < 20
FENA: 20
445
Describe the urine osmolarity, urine sodium, FENA, and serum BUN/Cr seen in intrinsic azotemia?
Urine osmolarity: 40
FENA: >2%
Serum BUN/Cr: < 15
446
Describe the urine osmolarity, urine sodium, FENA, and serum BUN/Cr seen in postrenal azotemia?
Urine osmolarity: 40
FENA: >2%
Serum BUN/Cr: >15
447
What are some commonly seen things in renal failure?
```
Hyperkalemia, hypocalcemia
Metabolic acidosis
Uremia (increased BUN and creatinine)
Anemia
Renal osteodystrophy
Dyslipidemia
Hyperphosphatemia
```
448
What is renal osteodystrophy?
Failure of vitamin D hydroxylation, hypocalcemia, and hyperphosphatemia leading to secondary hyperparathyroidism
449
What is seen in renal osteodystrophy?
Hyperphosphatemia can independently decreased serum calcium but causing tissue calcifications, whereas decreased vitamin D leads to decreased intestinal calcium absorption
causes subperiosteal thinning of bones
450
A patient presents with flank pain, hematuria, hypertension, urinary infection and progressive renal failure - what disease do they have?
ADPKD
451
What is ADPKD?
Multiple, large bilateral cysts that ultimately destroy the kidney parenchyma
452
What is the mutation in ADPKD?
AD mutation in PKD1 or PKD2
453
What 3 findings are associated with ADPKD?
Berry aneurysms
mitral valve prolapse
benign hepatic cysts
454
What causes death in patients with ADPKD?
death from complications of chronic kidney disease or hypertension (caused by increased renin)
455
What is ARPKD?
Infantile presentation in parenchyma
| significant renal failure in utero can lead to Potter's syndrome
456
What is ARPKD associated with?
congenital hepatic fibrosis
457
What are the concerns with ARPKD beyond the neonatal period?
hypertension, portal hypertension, progressive renal insufficiency
458
What is medullary cystic disease?
inherited disease causing tubulointerstital fibrosis and progressive renal insufficiency with inability to concentrate the urine
has poor prognosis
459
What is seen on PE with medullary cystic disease?
medullary cysts usually no visualized but shrunken kidneys can be seen on ultrasound
460
What part of the kidney does mannitol and acetazolamide work?
Proximal convoluted tubule
461
What is the MOA of mannitol?
Causes increased serum osmolarity so it acts as an osmotic diuretic, causes increased tubular fluid osmolarity producing increased urine flow
also decreases intracranial and intraocular pressure
462
What are the clinical uses of mannitol?
Drug overdose, elevated intracranial/intraocular pressure
463
What is the MOA of acetazolamide?
Carbonic anhydrase inhibitor
464
What does Acetazolamide cause?
self limited sodium bicarcb diuresis and reduction in total body bicarb stores
465
What are the clinical uses of Acetazolamide?
- Chronic glaucoma (bicarb helps to pull fluid into the eye to make aqueous humor)
- Urinary alkalinization
- altitude sickness
- metabolic alkalosis
- pseudotumor cerebri
466
What are the side effects seen with Mannitol?
Pulmonary edema, dehydration
| note mannitol is contraindicated in anuria (renal failure) and CHF
467
What are the side effects seen with Acetazolamide?
Hyperchloremic metabolic acidosis, paresthesias, NH3 toxicity, sulfa allergy
"ACID"azolamide causes ACIDoses
468
Where do loop diuretics like Furosemide and ethacrynic acid have their effects?
thick ascending limb of loop of henle
469
What is the MOA of Furosemide?
- Inhibits cotransport system (Na, K, 2CL) of thick ascending limb of loop of Henle.
- Abolishes hypertonicity of the medulla preventing concentration of urine
- Stimulates PGE release (vasodilatory effect on afferent arteriole), inhibited by NSAIDS
- Increases calcium excretion ( LOOPS LOSE CALCIUM!)
470
What is the clinical use of Furosemide?
Edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema), hypertension, hypercalcemia
471
What is the problem with Furosemide?
It's a sulfonamide!
472
What is the toxicity seen with furosemide?
```
LOOPS? OH DANG!
Ototoxicity
Hypokalemia
Dehydration
Allergy (sulfa)
Nephritis (interstitial)
Gout
```
473
What is Ethacrynic acid and it's MOA?
It's a loop diuretic but it's not a sulfa drug, instead it's a penoxyacetic acid derivative
it has essentially the same action as furosemide
474
What's the clinical use of Ethacrynic acid?
diuresis in patients allergic to sulfa drugs
475
What is the toxicity seen in Ethycrynic acid?
Similar to furosemide, can cause hyperuricemia
| never use to treat gout!
476
Where in the nephron does Hydrochlorothiazide work?
Distal convoluted tubule
477
What is the MOA of thiazides?
Inhibits NaCl reabsorption in the early distal tubule, reducing diluting capacity of the nephron
478
What's the difference between thiazides in loop diuretics when it comes to calcium?
Loops LOSE calcium and thiazides retain calcium
479
What are the clinical uses of thiazides?
HYPERTENSION!
| CHF, idiopathic hypercalciuria, nephrogenic diabetes insipidus
480
What are the toxicities seen with thiazide diuretics?
Hypokalemic metabolic alkalosis
hyponatremia
```
HyperGLUC
hyperGlycemia
hyperLipidemia
HyperUricemia
hyperCalcemia
```
note that thiazide diuretics are sulfa drugs!
481
Name 4 potassium sparing diuretics
"Potassium, please have a SEAT"
Spironolactone
Eplerenone
Amiloride
Triamterene
482
What is the MOA of spironolactone and eplerenone?
competitive aldosterone receptor antagonists in the cortical collecting tubule
483
What is the MOA of triamterene and amiloride?
Act in the cortical collecting tubule to block sodium channels ( block eNaC)
484
What is the clinical use of potassium sparing diuretics?
Hyperaldosteronism, Potassium depletion, CHF
you can give it with a loop diuretic to retain potassium
485
What is the toxicity seen with potassium sparing diuretics?
Hyperkalemia that can lea to arrhythmias
| endocrine effects with spironolactone (gynecomastia, antiandrogen effects)
486
Why don't you see antiandrogen effects with eplerenone like you do with spironolactone?
Eplerenone is more specific for the mineralocorticoid receptor
487
Diuretic effects on urine NaCl?
Increased with all diuretics except acetazolamide
| Serum sodium may decrease as well
488
Diuretic effects on urine K+?
Increased in all except potassium sparing diuretics
| serum potassium may decrease as well
489
Why do you see metabolic acidosis with carbonic anhydrase inhibitors and with potassium sparing diuretics?
Carbonic anhydrase inhibitors - decrease bicarb reabsorption
Potassium sparing diuretics - aldosterone blockade prevents K secretion and H+ secretion. Additionally, hyperkalemia lead to K entering all cells (via H/K exchanger) in exchange for H exiting the cells
490
Why do you see metabolic alkalosis in thiazides and loop diuretics?
Several mechanisms:
- Volume contraction leads to increased ATII which leads to increased Na/H exchange in proximal tubule leading to increased bicarb reabsorption (contraction alkalosis)
- K loss leads to K exiting cells in exchange for H entering cells
- In low K state, H (rather than K) is exchanged for Na in cortical collecting tubule leading to alkalosis and paradoxical aciduria
491
why do you lose calcium with loop diuretics?
decreased paracellular calcium reabsorption
492
Why do thiazides retain calcium?
enhanced paracellular calcium reabsorption in proximal tubule and loop of henle
493
Name 3 ACE inhibitors
Captopril, Enalapril, lisinopril
494
in what patients should you avoid using ACE-I?
Patients with bilateral renal artery stenosis because ACE inhibitors will further decreased GFR which can lead to renal failuer
495
what is the MOA of ACE inhibitors?
Inhibit ACE leading to decreased ATII leading to decreased GFR by preventing constriction of efferent arterioles.
Levels of renin increase as a result of loss of feedback inhibition. Inhibition of ACE also prevents inactivation of bradykinin, a potent vasodilator
496
list 5 uses of ACE-I?
```
Hypertension
CHF
proteinuria
diabetic renal disease
Prevents unfavorable heart remodeling as a result of chronic hypertension
```
497
why are ACE-I beneficial in patients with diabetic renal disease?
decreases progression of proteinuria and progression of diabetic nephropathy
498
List the toxicities of ACE-I
```
Captopril's CATCHH
Cough
Angioedema
Teratogen (fetal renal abnormalities)
Creatinine increase (Decreased GFR)
Hyperkalemia (really only a big deal if you also have you patient on regular doses of aspirin or a potassium sparing diuretic)
Hypotension
```
499
What is Aliskiren?
Renin inhibitor. ONLY indicated for HTN
Can cause hyperkalemia and renal insufficiency
contraindicated in pregnancy
