Renal - Miscellaneous Flashcards
1
Q
What are the general symptoms of glomerulonephritis?
A
Hematuria, proteinuria, decreased GFR, HTN
2
Q
What are the general symptoms of nephrotic syndrome?
A
Hypoalbuminemia, edema, hyperlipidemia, fatty casts, proteinuria >3.5g/24hr
3
Q
What are the general symptoms of nephritic syndrome?
A
Hematuria, azotemia, HTN, oliguria, subnephrotic range proteinuria
4
Q
Normal GFR = ?
A
> 90 mL/min
5
Q
Normal urine output = ?
A
1500 mL/24 hr
6
Q
Normal urine protein = ?
A
<150 mg/24 hr
7
Q
Normal FeNa = ?
A
1%
8
Q
Normal FeUrea = ?
A
35%
9
Q
Normal specific gravity = ?
A
1.003-1.030
10
Q
Normal urine pH = ?
A
5-8
11
Q
Normal # of RBC on microscopy = ?
A
0-2/hpf
12
Q
Normal # of WBC on microscopy = ?
A
0-5/hpf
13
Q
Oliguria = ?
A
<500 mL/24 hr
14
Q
Polyuria = ?
A
> 3000 mL/24 hr
15
Q
Anuria = ?
A
0 mL/24 hr
16
Q
Dysmorphic RBCs indicate an issue with…
A
Glomeruli
17
Q
RBC casts indicate ___.
A
Glomerulonephritis
18
Q
WBC casts indicate ___.
A
Pyelonephritis
19
Q
Epithelial (muddy brown) casts indicate ___.
A
Acute tubular necrosis
20
Q
Fatty casts indicate ___.
A
Nephrotic syndrome
21
Q
Granular casts indicate ___.
A
CKD (or non-specific)
22
Q
Hyaline casts indicate ___.
A
Dehydration, exercise, diuertics
23
Q
Waxy casts indicate ___.
A
Advanced kidney disease
24
Q
GFR = ?
A
([U] x V)/[P]
25
Cockcroft Gault equation - GFR = ?
((140 - age) x weight (kig) x 0.85 if female)/(72 x serum creatinine)
26
FeNa = ?
(UNa/PNa)/(UCr/PCr) x 100
27
What is a normal FF?
20%
28
What is the normal RPF?
625 mL/min
29
What is a normal urine Na?
20 mEq/L
30
Compare the urine Na+ in a pre-renal and renal issue.
Pre-renal: <20 mmol/L
| Renal: >20 mmol/L
31
Compare the FeNa and FeUrea in a pre-renal and renal issue.
Pre-renal: <1%
| Renal: >1%
32
Compare the urine specific gravity in a pre-renal and renal issue.
Pre-renal: >1.015
| Renal: ~1.010
33
Compare the urine osmolality in a pre-renal and renal issue.
Pre-renal: >350 mmol/kg
| Renal: <350 mmol/kg
34
Compare the casts seen in a pre-renal, renal, and post-renal issue.
Pre-renal: hyaline
Renal: Granular
Post-renal: hyaline
35
Compare the U/P creatinine ratio in a pre-renal and renal issue.
Pre-renal: >40
| Renal: <20
36
Compare the serum BUN/Cr ratio in a pre-renal and renal issue.
Pre-renal: >20:1
| Renal: <10:1
37
What are the symptoms of nephritic syndrome?
Acute onset of hematuria (dysmorphic RBC, RBC casts), oliguria, azotemia, HTN, edema, mild proteinuria
38
What are the four types of nephritic syndrome?
1. Post-infectious GN
2. Ig-A nephropathy
3. Hereditary nephritis
4. Rapidly progressive GN
39
What is systemic IgA nephropathy?
HSP
40
What are the symptoms of nephrotic syndrome?
Massive proteinuria (>3.5 g), hypoalbuminemia, generalized edema, hyperlipidemia, lipiduria
41
What are the three types of primary nephrotic syndrome?
1. Membranous nephropathy
2. Minimal change disease
3. FSGS
42
What are the two types of nephrotic syndrome with hematuria?
1. Membranoproliferative glomerulnephritis
| 2. Dense deposit disease
43
If pH <5, think ___.
Metabolic acidosis
44
If pH >5.3 in the presence of metabolic acidosis, think ___.
Distal RTA
45
If pH >8, think ___.
Presence of urea-splitting organisms
46
A specific gravity of 1.001 is very ___ and a specific gravity of 1.030 is very ___.
Dilute; concentrated
47
What does a specific gravity of 1.010 indicate?
Urine is neither concentrated nor dilute
48
If there is an acute decline in renal function and specific gravity is > 1.020, think ___.
Pre-renal issue (urine can still be concentrated)
49
If there is an acute decline in renal function and specific gravity is ~1.010, think ___.
Renal issue (urine can no longer be concentrated)
50
If there is hyponatremia, normally expect a ___ specific gravity. If there is hypernatremia, normally expect a ___ specific gravity.
Low; high
51
If specific gravity is > 1.010 in the setting of hyponatremia, think ____.
ADH secretion is occurring (urine is being concentrated)
52
If specific gravity is <1.010 in the setting of hypernatremia, think ___.
Diabetes inspidius (urine is being diluted)
53
If there is elevated blood glucose and glycosuria, think ___.
Diabetes mellitus
54
If there is normal blood glucose and glycosuria, think ___.
Proximal tubule dysfunction
55
If there is ketoacidosis and ketonuria, think ___.
Diabetic or alcoholic ketoacidosis
56
If there is no ketaocidosis and ketonuria, think ___.
Starvation, ketogenic diet, isopropyl alcohol ingestion
57
If there is bilirubin in the urine, think ___.
Hepatobiliary disease
58
If there is bilirubin in the urine without urobilinogen, think ___.
Biliary obstruction
59
If there is urobilinogen in the urine, think ___.
Liver disease
60
If there is leukocyte esterase or nitrites in the urine, think ___.
UTI
61
Compare the presentations of of the 4 types of nephritic syndrome.
1. Acute post-infectious GN: Hematuria, edema, HTN, renal failure within 1-4 weeks of a throat/skin infection (presentation less clear in adults)
2. IgA nephropathy: recurrent, often painless hematuria within 1-2 days of an upper respiratory, GI, or urinary infection, proteinuria
3. Hereditary nephritis: isolated hematuria, nephritis, no infection, hearing issues and ocular issues
4. Rapidly progressive GN: rapidly progressive loss of renal function, nephritic syndrome
Type I - gross hematuria, oliguria, hemoptysis
Type II - gross hematuria, oliguria
Type III - gross hematuria, oliguria, hemoptysis/SOB
62
Compare the epidemiology of the 4 types of nephritic syndrome.
1. Acute post-infectious GN: children 6-10 y/o (rare in adults)
2. IgA nephropathy: most common glomerular disease, children and adults
3. Hereditary nephritis: 5-20 y/o males (age of presentation)
4. Rapidly progressive GN:
Type I - young men
Type II - older children/young adults
Type III - older adults
63
Compare the etiology/pathogenesis of the 4 types of nephritic syndrome.
1. Acute post-infectious GN: formation of Ag/IgG IC in circulation, deposition of IC in capillary wall, complement activation, influx of neutrophils, damage and endocapillary proliferation + in-situ IC formation
2. IgA nephropathy: infection causes massive IgA production, IgA/Complement IC formation, deposition in mesangium, alternative complement pathway activated
3. Hereditary nephritis: error in collagen type IV synthesis (affects GBM, cochlea, lens)
4. Rapidly progressive GN:
Type I - anti-glomerular basement membrane Ab
Type II - IC formation, necrosis and breaks in glomerular BM
Type III - ANCA (Ab to neutrophilic granules)
64
Compare the histology, IF, and EM images of the 4 types of nephritic syndrome.
1. Acute post-infectious GN: Histology - capillary obliteration, endocapillary proliferation, PMN influx; EM - humps; IF: IgG + Ag/Complement
2. IgA nephropathy: Histology - mesangial proliferation, EM - electron dense deposits; IF - IgA + complement/auto-Ab
3. Hereditary nephritis - Histology - normal; EM - basket weave (lamina densa splitting); IF - negative
4. Rapidly progressive glomerulonephritis - All types - Histology: crescents
Type I: IF - linear IgG, EM - none
Type II: IF - granular deposits (Ig + complement), EM - electron dense deposits
Type III: IF - pauci immune, EM - pauci immune
65
What other lab tests are important in acute post-infectious GN?
1. ASO titer increases
2. Complement decreases
3. Coca-cola, tea-colored urine
66
What other lab tests are important in IgA nephropathy?
1. No decrease in complement
67
Describe the IgA nephropathy with extra-renal symptoms (systemic IgA).
Henoch Schonlein Purpura
Mainly seen in 3-8 y/o
IC deposits in kidney (hematuria), skin (purpuric skin lesions), GI (abdominal pain and GI bleeding), and joints (arthralgia)
68
Which nephritic syndromes do not involve immune complexes?
Hereditary nephritis
| Type I and III rapidly progressive GN
69
What is Goodpasture disease?
Type I rapidly progressive GN + alveolar basement membrane involvement
70
What is the antigen attacked in Goodpasture disease?
NC1 (non-collagenous protein)
71
What triad is commonly affected in GPA? What type of ANCA and antigen are involved?
Ear/nose throat
Lungs
Kidney
c-ANCA, PR3
72
Compare the presentations of of the 3 types of nephrotic syndrome.
All three: nephrotic syndrome
1. Membranous nephropathy: edema, thrombosis (loss of AT-III), infection
2. Minimal change disease: edema
3. FSGS: hematuria, reduced GFR, HTN
73
Compare the epidemiology of the 3 types of nephrotic syndrome.
1. Membranous nephropathy: 30-60 y/o, second most common nephrotic syndrome
2. Minimal change disease: 2-6 y/o, most common nephrotic syndrome in children, adults (10%)
3. FSGS: adults (most common nephrotic syndrome) and children
74
Compare the etiology/pathogenesis of the 3 types of nephrotic syndrome.
1. Membranous nephropathy: autoimmune response against renal Ags, IC formation, podocyte injury, NO inflammatory response, often associated with cancer
2. Minimal change disease: reversible podocyte injury
3. FSGS: irreverisble podoctye injury, leads to sclerosis and lumen obliteration
75
Compare the histology, IF, and EM images of the 3 types of nephrotic syndrome.
1. Membranous nephropathy: Histology - normal; EM - subepithelial electron dense deposits, IF - granular deposits (IgG and C3); silver stain - spike and dome pattern (basement membrane positive - black)
2. Minimal change disease: Histology - normal; EM - effacement/fusion of podocyte foot processes; IF - none
3. FSGS: Histology - segemental sclerosis; EM - effacement of podocytes in all glomeruli; IF - none.
76
What are the two renal antigens targeted in membranous nephropathy?
PLA2R, THSD7A
77
What other lab tests are important in membranous nephropathy?
1. Ab testing for PLA2R, THSD7A
| 2. No drop in complement
78
If you have membranous nephropathy, you must rule out ___.
Cancer
79
Discuss steroid treatment of minimal change disease and FSGS.
Minimal change disease responds to steroids. FSGS initially responds to steroids but may become resistant.
80
What are the three common etiologies of FSGS?
1. Primary (idiopathic)
2. Adaptive (response to nephron loss)
3. APOL1 (risk alleles)
81
What are the three uncommon etiologies of FSGS?
1. Genetic
2. Medication-associated
3. Virus-associated
82
Compare the etiology/pathogenesis of the 2 nephrotic/nephritic syndromes.
1. MPGN: IC formation with classical complement activation
| 2. DDD: sustained activation of the alternative complement pathway (non-antibody mediated)
83
Compare the histology, IF, and EM images of the 2 types of nephrotic/nephritic syndrome.
1. MPGN: Histology - lobular tufts; EM - electron dense deposits and tram tracks; IF - IgG + complement; silver stain - tram tracks
2. DDD: Histology - none mentioned; EM - dense deposits in lamina densa; IF - C3 (no Ig)
84
What are the two major control points affecting the complement pathway in DDD?
1. C3NeF is an autoantibody against C3 convertase - it stabilizes the enzyme and prevents its degradation
2. H factor normally degrades C3 convertase; mutations/autoantibodies diminish its ability to do so
85
What is an important drug treatment for DDD?
Eculizumab
86
What are three systemic kidney issues and how are they categorized (nephrotic/nephritic)?
Nephrotic: diabetic nephropathy, amyloidosis
Nephritic: lupus nephritis (can be nephrotic 10% of the time)
87
What are the symptoms of diabetic nephropathy?
1. Proteinuria
2. Progressive decrease in GFR
3. HTN
88
What important histologic finding is seen in diabetic nephropathy?
KW nodules (thickening of GBM, increased mesangial matrix)
89
Discuss the clinical presentation of TMAs.
1. Microangiopathic hemolytic anemia
2. Thrombocytopenia and thrombi in microcirculation
3. Renal failure
4. Diarrhea (HUS only)
90
Discuss the lab tests for TMA.
1. Thrombi and endothelial injury in histology
2. Thrombocytopenia
3. Schistocytes on blood smear
4. ADAMTS13 mutation
91
What are the two major categories of tubulointerstitial diseases?
1. Tubulointerstitial nephritis
| 2. Acute tubular injury/necrosis
92
What are the primary types of tubulointerstitial nephritis?
Infectious: pyelonephritis (acute, chronic, papillary necrosis, viral, xanthogranulomatous)
Non-infectious:
1. Acute drug-induced (particularly NSAIDs, aristolcholic acid)
2. Metabolic (urate and oxalate nephropathies)
3. Neoplasm (multiple myeloma - uric acid, hypercalcemia, light chain casts)
93
What are the two major causes of acute tubular injury/necrosis?
Ischemia and toxins
94
Compare acute and chronic pyelonephritis on histology.
Acute: patchy interstitial suppurative inflammation (PMNs)
Chronic: lymphocytes, fibrosis, sclerosis, dilated tubules
95
What are the 4 broad causes of pre-renal AKI?
1. Absolute decrease in ECV
2. Relative decrease in ECV
3. Low ECV + impaired renal autoregulation
4. Vasoconstriction and occlusion
96
What causes an absolute decrease in ECV?
Vomiting, diarrhea, hemorrhage
97
What causes a relative decrease in ECV?
HF, cirrhosis
98
What causes low ECV + impaired renal autoregulation?
NSAIDs, ACEI/ARB
99
What causes vasoconstriction and occlusion?
Hypercalcemia, chemo, renal artery stenosis
100
What are some exogenous toxins that can cause acute tubular necrosis?
Antibiotics, chemotherapy, contrast, mannitol
101
What are some endogenous toxins that can cause acute tubular necrosis?
Myoglobin (rhabdo), uric acid (tumor lysis), light chains (myeloma), hemoglobin (hemolysis)
102
What is the classic triad of symptoms seen in acute interstitial nephritis?
Fever, rash, eosinophilia
103
What are the clinical features of contrast nephropathy?
1. Increase in serum creatinine 2-3 days after contrast administration
2. Non-oliguric
3. Pre-renal urine indices, high specific gravity
4. ATN eventually
104
What are some causes of high BUN?
1. Pre-renal issue
2. High dose steroids
3. Hyper-catabolic states (fever, burns)
4. High protein diet
5. GI bleed
105
What are some causes of low BUN or creatinine?
1. Low protein diet
2. Cachetic patients
3. Cirrhosis (high bilirubin interferes with measurement)
106
What are some causes of high creatinine?
1. High muscle mass
2. Creatinine supplements
3. Rhabdomyolysis
4. Diet high in animal protein
5. Drugs blocking tubular secertion
6. Measurement issues
107
What are the general indications for dialysis?
1. Acidosis
2. Electrolytes (hyperkalemia)
3. Intoxication (salicylate, lithium, isopropanol, methanol, ethylene glycol)
4. Overload (volume)
5. Uremia
108
What are the 4 congenital renal abnormalities?
1. Agenesis
2. Hypoplasia
3. Ectopic
4. Horseshoe
109
What causes renal dysplasia?
Immature elements in metanephric development
Leads to noncommunicating cysts of various sizes separated by dysplastic parenchyma and the absence of a normal pelvocaliceal system; associated with ureteral or ueteropelvic atresia
110
What is the gross and histologic appearance of renal dysplasia?
Bunch of grapes; cartilage on histology
Can be uni/bilateral, non-reniform, can be segmental
111
What gene is mutated in AR PCKD and what does it encode?
PKHD1 (encodes fibrocystin)
112
What is the gross and histologic appearance of AR PCKD?
Gross: enlarged bilateral reniform kidneys
Histology: sponge-like cross section, dilated tubules
113
What is the gross and histologic appearance of AD PCKD?
Gross: giant kidney
Histology: cysts, functioning nephrons
114
What two complications are associated with AD PCKD?
Intracranial berry aneurysm, mitral valve prolapse
115
What are the two benign adult renal tumors?
1. Oncocytoma
| 2. Angiomyolipoma
116
What is the classic symptom triad of RCC?
1. Painless hematuria
2. Palpable abdominal mass
3. Dull flank pain
117
Describe the pathogenesis of clear cell type RCC.
Loss of 3p leads to VHL inactivation; normally, VHL breaks down HIF-1a; when VHL is inactivated, HIF-1a increases and leads to tumor cell survival
118
Describe the gross and histologic presentation of clear cell RCC.
Gross: yellow-orange, adrenal-like tumor
Histology: chicken-wire, clear cytoplasm, highly vascularized
119
Describe the symptoms of Beckwith-Widemann syndrome.
1. Wilms tumor
2. Macroglossia
3. Organomegaly
4. Hemihypertrophy
120
Describe the symptoms of the WAGR complex.
1. Wilms tumor
2. Aniridia (absence of iris)
3. Genital abnormalities
4. mental Retardation
121
Describe the symptoms of Denys-Drash syndrome.
1. Wilms tumor
2. Gonadal dysgenesis
3. Renal mesangial sclerosis
122
What is the cause of Wilms tumors?
Recapitulating nephrogenesis
123
Describe the histologic triphasic presentation of Wilms tumors.
1. Undifferentiated blastoma
2. Tubules
3. Fibroblast-like stroma
124
Which renal tumor is chemo resistant? Chemo sensitive?
Resistant: RCC
Sensitive: Wilms tumor
125
Membranoproliferative GN is associated with what illness?
Hepatitis C
126
What are the consequences of renal failure?
MAD HUNGER
```
Metabolic Acidosis
Dyslipidemia
Hyperkalemia
Uremia
Na/H2O retention
Growth retardation/developmental delay
Erythropoietin defiency
Renal osteodystrophy
```
127
How is stage II/III CKD managed?
Healthy living, treat co-morbid disorders, avoid NSAIDs
128
How is stage III-V CKD managed?
Refer to nephrology, control HTN (low sodium diet), reduce proteinuria
129
How is stage IV-V CKD managed?
1. Manage mineral and bone disorders
2. Manage anemia
3. Manage metabolic acidosis
130
What are the aspects of uremic cardiovascular disease?
1. Medial vascular calcification
2. Arterial stiffness
3. LV hypertrophy
4. Increased risk of cardiac arrest and HF
131
pH = ?
pKa + log [A-]/[HA] = -log[H+]
132
For each 0.3 increase in pH, what happens to [H+]?
Halved
133
What happens in metabolic acidosis?
Primary decrease in [HCO3-], relative increase in [H+], compensatory respiratory alkalosis (hyperventilation)
134
What are causes of increased anion gap acidosis?
1. Increased acid production/acid retention (ketoacidosis, lactic acidosis, toxin ingestion - salicylate, methanol, ethylene glycol)
2. Failure to excrete inorganic anions (renal failure)
135
What are causes of normal anion gap acidosis?
1. GI loss of [HCO3-] via diarrhea
2. Renal loss of [HCO3-] via proximal RTA, CA inhibitors
3. Failure to excrete acid via distal RTA
4. Administration of acid or saline
136
What happens in metabolic alkalosis?
Primary increase in [HCO3-], relative decrease in [H+], compensatory respiratory acidosis (hypoventilation)
137
What are 3 general causes of metabolic alkalosis?
1. Net H+ loss from ECF
2. Net HCO3- addition to ECF
3. Cl- depletion
138
What are 3 causes of H+ loss from ECF?
1. GI loss (vomiting)
2. Renal loss (mineralocorticoid excess, diuretics, increased Na+ distal tubule delivery)
3. Movement to ICF (hypokalemia)
139
What causes net bicarbonate addition to ECF?
Exogenous administration of bicarbonate, lactate, citrate, acete
140
What are 2 causes of GI Cl- depletion?
1. Secretion into stool (villous adenoma)
| 2. Reabsorption failure (congenital chloridorrhea)
141
What are 3 causes of renal Cl- depletion
1. Diuretics
2. Bartter's syndrome (defect of Na/K/2Cl transporter)
3. Gitelman's syndrome (defect of NaCl transporter)
142
What is 1 cause of skin Cl- depletion?
Cystic fibrosis
143
What causes maintenance of alkalosis broadly?
Net failure to excrete bicarbonate
144
What are 4 causes of alkalotic maintenance?
1. ECF depletion, decreased GFR, increased proximal tubule bicarbonate reabsorption
2. Cl depletion, increased distal tubule bicarbonate reabsorption/decreased distal secretion
3. Potassium depletion (lower intracellular pH, stimulate bicarbonate reabsorption)
4. Hypercapnea (increased PCO2 decreases intracellular pH, stimulates bicarbonate reabsorption)
145
Define chloride resistant alkalosis.
Urine chloride is high, >20 mmol/L, low renin
146
Define chloride responsive alkalosis.
Urine chloride is low, <10 mmol/L, high renin
147
How is metabolic alkalosis treated?
1. Potassium
2. Acetazolamide
3. Volume repletion
4. IV HCl or NH4Cl
148
Anion gap = ?
Na - Cl - HCO3
149
Normal AG = ?
10-12 mEq/L
150
What pH indicates acidosis? Alkalosis?
Acidosis: <7.35
Alkalosis: >7.45
151
If acidotic, what indicates metabolic versus respiratory?
Metabolic: HCO3- <22 mEq/L
Respiratory: PCO2 >45 mm Hg
152
If metabolic acidosis, what indicates respiratory compensation?
PCO2 < 35 mm Hg
153
If respiratory acidosis, what indicates renal compensation?
HCO3- >28 mEq/L
154
If alkalotic, what indicates metabolic versus respiratory?
Metabolic: HCO3- >28 mEq/L
Respiratory: PCO2 <35 mm Hg
155
If metabolic alkalosis, what indicates respiratory compensation?
PCO2 > 45 mm Hg
156
If respiratory alkalosis, what indicates renal compensation?
HCO3- <22 mEq/L
157
Calculate predicted compensation - metabolic acidosis.
Delta PCO2 = 1.2(Delta HCO3-)
158
Calculate predicted compensation - metabolic alkalosis.
Delta PCO2 = 0.7(Delta HCO3-)
159
Calculate predicted compensation - acute respiratory acidosis.
Delta HCO3- = 0.1(Delta PCO2)
160
Calculate predicted compensation - chronic respiratory acidosis.
Delta HCO3- = 0.4(Delta PCO2)
161
Calculate predicted compensation - acute respiratory alkalosis.
Delta HCO3- = 0.2(Delta PCO2)
162
Calculate predicted compensation - chronic respiratory alkalosis.
Delta HCO3- = 0.4(Delta PCO2)
163
What happens in Type I RTA?
Distal - intercalated cells cannot secrete H+
| Urine pH >5.5
164
What happens in Type II RTA?
Proximal - defective PT HCO3- reabsorption
| Urine pH <5.5
165
What happens in Type IV RTA?
Hypoaldosteronism
| Urine pH <5.5
166
What are the shapes of calcium oxalate stones?
Envelopes and dumbbells
167
What is the shape of calcium phosphate stones?
Wedge prisms and needles
168
What are the shapes of uric acid stones?
Rhomboids or rosettes
169
What are the shapes of struvite stones?
Staghorn calculi or coffin lids
170
What is the shape of cystine stones?
Hexagonal on micro
171
What causes hypovolemic hyponatremia?
Decreased TBW with greatly decreased TBNa+
Diuretics, Addison's disease, salt wasting, diarrhea, vomiting, sweating
172
How is hypovolemic hyponatremia treated?
Physiologic saline
173
What causes euvolemic hyponatremia?
Increased TBW with normal TBNa+
SIADH, hypothryoidism, psychogenic polydipsia, beer drinking podomania
174
How is euvolemic hyponatremia treated?
Water restriction if severe; if symptomatic, give hypertonic saline +/- diuretics
175
What causes hypervolemic hyponatremia?
Greatly increased TBW with increased TBNa+
CHF, cirrhosis, renal failure
176
How is hypervolemic hyponatremia treated?
Fluid restriction and diuretics
177
What causes hypovolemic hypernatremia?
Greatly decreased TBW with decreased TBNa+
Diuretics without water intake, tubular injury, sweating, diarrhea, vomiting with inadquate water intake
178
How is hypovolemic hypernatremia treated?
Hypotonic fluid administration
179
What causes euvolemic hypernatremia?
Decreased TBW with normal TBNa+
Central and nephrogenic diabetes insipidus, decreased thirst/water intake
180
How is euvolemic hypernatremia treated?
Water administration, ADH administration in central DI
181
What causes hypervolemic hypernatremia?
Normal TBW with increased TBNa+
Hypertonic fluid administration, mineralocorticoid excess, salt poisoning
182
How is hypervolemic hypernatremia treated?
Water administration + diuretics or dialysis to remove Na+; rate of correction should not exceed 0.5 mEq/L/hr, can lead to brain edema
183
What is a normal plasma sodium range?
135-145 mEq/L
184
What is normal urinary Na+?
10-20 mmol/L
185
What are the two most common adherence factors in E. coli, what do they bind to, and where are they found?
1. Type 1 Fim H - bind to D-mannose on epithelial cells in bladder and lower tract
2. PAP - p fimbriae - bind to P blood group Ag in renal pelvis and kidney
186
What are the two protective urine properties?
1. IgA/IgG
| 2. Tamm-Horsfall protein
187
What are first line treatment for uncomplicated cystitis?
1. Nitrofurantoin, bactrim, fosfacmyin
| FQ - 2, oral beta-lactams - 3
188
What are first line treatment for uncomplicated pyelonephritis?
FQ, Bactrim
189
What are intraluminal causes of obstruction?
Renal calculi, blood clots, sloughed renal papilla, urothelial tumors, fungal ball
190
What causes sloughed renal papilla?
Diabetes, sickle cell, pyelonephritis, phentactein abuse
191
What are intramural causes of obstruction?
UPJ obstruction, structural lesions
192
What are extramural causes of obstruction?
Prostate disease, cancer, crossing vessels, retroperitoneal fibrosis
193
What are the 3 functional changes in unilateral obstruciton?
1. Increased ureteral pressure decreases GFR; this decreases Na+ delivery to the macula densa. Afferent arteriole dilates to increase RBF and GFR
2. Ureteral pressure continues to increase; efferent arteriole constricts, decreasing RBF and increasing GFR
3. Ureteral pressure and RBF decrease due to decreased GFR and afferent arteriole constriction?
194
What are the three most common sites of obstructions?
1. Junction between ureter and bladder
2. UPJ
3. Where ureter crosses iliac muscles
195
What are the 11 symptoms of lupus?
1. Serositis
2. Oral ulcers
3. Arthritis
4. Photosensitivity
5. Blood disorder
6. Renal disorder
7. ANA
8. Immunologic abnormalities
9. Neurological symptoms
10. Malar rash
11. Discoid rash
196
What are the 5 types of lupus?
SLE, discoid, drug-induced, neonatal, overlap with another AI disease
197
What are the important lab tests for lupus?
1. ANA (sensitive)
2. Anti-DsDNA (specific)
3. Anti-Smith
4. Decreased C3 and C4
198
What are the symptoms of Sjogren's syndrome?
Exocrine glandular dysfunction due to lymphocytic infiltration
1. Xerophthalmia (dry eyes)
2. Xerostomia (dry mouth)
3. Vaginal and skin dryness, constipation
4. Parotid enlargement
5. Joint pain
199
What are the important lab tests for Sjogren's syndrome?
1. Anti-SSA/SSB
2. Rheumatoid factor
3. Renal tubular acidosis
200
What are the symptoms of systemic sclerosis (scleroderma)?
1. Raynaud
2. Skin tightening
3. Finger tip ulcers
4. Joint contractures
5. Renal HTN
6. Dyspnea
7. GERD
8. Diarrhea/malabsorption
9. Weight loss
201
What are the two subtypes of systemic sclerosis?
Diffuse and Limited
202
What are the symptoms of diffuse scleroderma?
Extensive skin involvement, interstitial lung disease, anti-topoisomerase I
203
What are the symptoms of limited scleroderma?
Limited skin involvement, CREST syndrome (Calcinosis, Raynaud, Esophageal dysmotility, Sclerodactylyl, Telangiectasia), pulmonary HTN, anti-centromere antibody
204
What antibody goes with scleroderma renal crisis?
Anti-RNA-polymerase III
205
What are the antibodies associated with anti-phospholipid syndrome?
aCL, anti-beta2-glycoprotein 1, lupus anticoagulant
206
Anti-phospholipid syndrome can cause a false positive ___.
VDRL/RPR test and a prolonged PTT
207
Chronic hyperphosphatemia leads to...
decreased renal activation of vitamin D and secondary hyperparathyroidism
208
FeNa should ___ as GFR decreases.
Increase
209
Describe the transporters in the cells of the PCT.
Lumen:
1. Na/H exchanger (Na into cell, H into lumen)
2. Cl/Base exchanger (Cl into cell, Base into lumen)
3. Reaction forming H2O + CO2 --> diffuses into the cell
Cell:
1. CO2 + H2O forms H2CO3 which forms H+ and HCO3
Blood:
1. Na/K ATPase (Na into blood, K into cell)
2. HCO3- transporter (into blood)
210
Describe the transporters in the cells of the TAL.
Lumen:
1. Na/K/2CL transporter (into cell)
2. K+ channel (into lumen)
3. Mg/Ca paracellularly into blood
Blood:
1. Na/K ATPase
2. K+ channel (into blood)
3. Cl- channel (into blood)
211
Describe the transporters in the cells of the DCT.
Lumen:
1. Na/Cl transporter (into cell)
2. Ca2+ channel (into lumen)
Blood:
1. Na/K ATPase
2. Na/Ca2+ exchanger (Na into cell Ca2+ into blood)
3. Cl- channel (into blood)
PTH Receptor
212
Describe the transporters in the cells of the principal cell of the CCT.
Lumen:
1. Cl- paracellular diffusion (into blood)
2. H2O channel (into cell)
3. K+ channel (into lumen)
4. Enac chanel (into cell)
Blood:
1. Na/K ATPase
ADH and Aldosterone receptors
213
Describe the transporters in the cells of the alpha-intercalated cell of the CCT.
Lumen:
1. H+ ATPase (into lumen)
2. K/H ATPase (K into cell, H into lumen)
Blood:
1. HCO3/Cl exchanger (HCO3- into blood, Cl- into cell)
Aldosterone receptor
214
Describe the transporters in the cells of the beta-intercalated cell of the CCT.
Lumen:
1. Cl/HCO3 exchanger (Cl into cell, HCO3 into lumen)
Blood:
1. H+ ATPase (into blood)
215
What is the prognosis of acute post-infectious GN?
Children - total recovery (95%)
Adults - slow progression to chronic GN (15-50% to ESRD)
Small subset of children and adults develop acute illness with gross hematuria and rapidly progressive renal failure
216
What is the treatment of acute post-infectious GN?
Supportive
217
True or false - IgA is a poor activator of the complement system.
True
218
What is the prognosis of IgA nephropathy?
Renal failure, rarely RPGN, HSP (kids, great prognosis)
219
What is the treatment of IgA nephropathy?
Supportive
220
What is the prognosis of hereditary nephritis?
Overt renal failure between 20-50 year of age
221
What is the treatment of hereditary nephritis?
Supportive, transplant
222
What is the prognosis of RPGN type I?
Renal and pulmonary failure
223
How is RPGN type I treated?
Plasmapheresis
224
What is the prognosis of RPGN type II?
Chronic renal failure
225
What is the treatment of RPGN type II?
Immunosuppression
226
What is the prognosis of RPGN type III/
Renal and pulmonary failure
227
What is the treatment of RPGN type III?
Immunosuppression
228
What type of ANCA and antigen are involved in EPGA?
p-ANCA, MPO
229
What is the prognosis of membranous nephropathy?
1/3 - spontaneous remission
1/3 - progress, require dialysis
1/3 - continued proteinuria, no progression
230
How is membranous nephropathy treated?
Immunosuppressive drugs, treatment of underlying disease (secondary), can recur after transplant
231
What is the prognosis of minimal change disease?
Several episodes of nephrotic syndrome, normal renal function, resolves at puberty
232
What is the treatment of minimal change disease?
Steroid sensitive
233
What is the prognosis of FSGS?
Progression to renal failure within 10 years
234
What is the treatment of FSGS?
Initially steroid-responsive, progresses to steroid resistant, recurs in transplant
235
What is the prognosis of MPGN?
Progression to renal failure
236
What is the treatment of MPGN?
Treat underlying disease
237
When a patient shows C3 by IF, but no DDD, what is this called?
C3 glomerulopathy
238
What is the prognosis of DDD?
Poor, progress to renal failure
239
What are the major differences between HUS and HSP?
HUS: thrombocytopenia, anemia with schisctocytes
HSP: rash/palpable purpura, joint pain/swelling
240
What are some things that can cause papillary necrosis?
1. Analgesics
2. Diabetes
3. Sickle cell anemia
4. Obstruction
5. TB
241
What is seen on a kidney biopsy of acute drug-induced interstitial nephritis?
Interstitial inflammation, abundant eosinophils, edema
242
What are the two aspects of the pathology of NSAID interstitial nephritis?
Interstitial nephritis and minimal change disease
243
How does acute tubular injury present?
Rapid reduction of renal function, oliguria, uremia, signs of fluid overload, electrolyte abnormalities, acidosis; can be non-oliguric 50% of the time
244
What is the most common cause of acute renal failure?
ATN
245
What are some causes of combined ATN?
1. Mismatched blood transfusion
2. Hemolytic crises
3. Skeletal muscle injury
4. Intratubular casts and crystals
246
Which of the 4 stones are radiolucent?
Uric acid (cystine mildly opaque)
247
Discuss the three phases of the clinical course of ATN.
1. Initiation (hours to days) - evolving tubular injury, potentiallyr eversible
2. Maintenance (1-2 weeks) - established renal injury, oliguria, epithelial casts
3. Recovery - repair and regeneration of tubules, polyuric
248
What genes are mutated in APKD?
1. PDK1 (earlier onset, more severe) - encodes polycystin 1, which regulates cell-cell interactions
2. PKD2 (later onset) - encodes polycystin 2, which regulates intercellular Ca2+
249
Describe oncocytoma on hsitology and EM.
Histology: eosinophilic cytoplasm
EM: abundant mito
250
What is mutated in angiomyolipoma?
TSC1 and TSC2
251
What is one possible targeted therapy for RCC, which is chemo-resistant?
mTOR inhibitors
252
Analgesic nephropathy is a risk factor for ___.
Urothelial carcinoma
253
Why are calcium oxalate stones related to hypocitraturia?
Citrate inhibits stone formation by forming a soluble complex with Ca2+
254
Why is vitamin C problematic for calcium oxalate stones?
Excess vitamin C is excreted in the oxalate form
255
How can calcium stones be prevented?
1. Low Na+
2. Normal dietary calcium
3. Thiazide diuretic (decrease calcium excretion)
4. Citrate
256
How can low citrate be corrected?
Lemon juice
257
How can uric acid stones be treated?
1. Give citrate to alkalinize urine
2. Give allopurinol, losartan
3. Lose weight
258
How can hyperoxaluria be addressed?
1. Low oxalate diet
2. Increase Ca2+
3. Calcium carbonate
4. Restrict vitamin C
259
How can cystine stones be treated?
Reduce supersaturation, give chelating agents
