Renal Flashcards
1
Q
Nephrotic syndrome key features
A
- Massive proteinuria (>3.5g/24h or 40mg/hr/m2 for children)
- Hypoalbuminemia (<30g/L)
- Generalized edema
- HL
2
Q
Nephrotic syndrome PE findings
A
- Periorbital edmea
- Ankle edema
- Muehrcke’s nails
- Xanthelasma
- Frothy urine
3
Q
S/S of CKD
A
- Fatigue
- Nocturia
- Thirst
- Fluid retention
- Itch
4
Q
Tx target of DM nephropathy
A
- Control HT, DM, HL
- ACEI for reducing proteinuria
- Anti-inflammatory/fibrosis
5
Q
Acidosis/Alkalosis on K
A
Acidosis –> HyperK
Alkalosis –> HypoK
6
Q
Normal pH / QM ref range
A
Normal pH: 7.35-7.45
[H] = 40nmol/L @ 7.4pH
7
Q
Acid/Alkalosis vs Acid/Alkalemia
A
- osis = a process
- emia = too much/too little H in blood
8
Q
Metabolic acidosis features
A
Decreased HCO3 (Normal: 22-28mmol/L) Hyperventilation to compensate
9
Q
Dx of Metabolic acidosis
A
Determine Anion gap
If high –> Done
If normal –> determine Urine anion gap
Look for any osmolar gap
10
Q
Normal value Anion gap
A
8-14
[Na - Cl - HCO3]
If normal AG –> Cl is increased
11
Q
Metabolic acidosis with increased AG
Causes
A
- DKA
- Alcoholic KA
- Lactic acidosis
- Renal failure
- Rhabdomyolysis
12
Q
Metabolic acidosis with normal AG
Causes
A
- HCO3 loss with compensatory Cl increase
- Diarrhea (GI loss), Proximal renal tubular acidosis (RTA; Renal loss)
- Failure to excrete H (Distal RTA / Type 4 RTA)
- Ingestion of NH4Cl
- Increased reabsorption of Cl (Ureterosignmoidostomy)
13
Q
Osmolar gap (OG) How to calculate
A
Actual - Calculated plasma osmolarity
Calculated = 2xNa + Urea + Glucose
Increased = Something osmolar inside, e.g. alcohol related compounds)
14
Q
Lactic acidosis type A and B
A
Type A
- Over-production --> O2 deficiency
- Causes:
Hypotension
Hypoxia
CO poisoning
Grand mal seizure
- Tx = Improve O2 delivery; NaHCO3 won't help unless controlled production; HD with HCO3 dialysis
Type B
- Reduced metabolism, w/o hypoxemia
- Liver problem, alcoholism, thiamine deficiency, Metformin
15
Q
Risk of NaHCO3 therapy
A
- HypoK (shifts K into cells)
- HypoCa
- Paradoxical cerebral acidosis if too rapid correction (CO2 can diffuse to brain but not HCO3)
- Volume expansion (from Na load)
16
Q
RTA (Renal tubular acidosis) types and features
A
Type 1
- Distal RTA (due to failure of H excretion)
- HypoK
- Acid loading test (NH4Cl): Urine cannot be acidified, pH remains >6.0 (N <5.5)
Type 2
- Proximal RTA (due to loss of HCO3)
- HypoK
- Fractional excretion of HCO3: Test for excessive loss of HCO3 in urine (>15%; cf <5% in Type 1)
Type 3
- Mixed
- HypoK
Type 4
- HyperK
- Aldo deficiency or resistance
17
Q
Mx of RTA
A
Type 1,2
- Oral NaHCO3 to correct acidosis (v high dose needed for Type 2; K citrate better for Type 1)
- K supplement for HypoK
- Distal RTA due to Sjogren’s –> Steroids
Type 4
- Stop / decrease inciting drugs
- Loop diuretics + low K diet for HyperK
18
Q
Causes of Metabolic alkalosis
A
H loss
- GI loss (Vomiting, Nasogastric drainage)
- Renal loss
- Diuretics, HypoK
- MC excess (Primary/Secondary)
- Bartter’s (looks like Loop diuretics) / Gitelman’s (looks like Thiazides)
HCO3 retention
- Intake of NaHCO3
- Milk-Alkali syndrome (taken too much Ca supplements / alkali for PU)
19
Q
Tx of Metabolic alkalosis
A
If ECF contracted –> Give Saline (HCO3 will fall with expansion)
IF ECF expanded –> IV HCl or Oral NH4Cl to correct alkalosis
Correct HypoK
20
Q
SIADH
A
Euvolemic hypoNa
Urine [Na] >20 mmol/L
Urine osmolarity >2x serum osmolarity
Tx
- Treat underlying cause (CNS/RS/Drugs)
If asymptomatic + Na>110
- Fluid restriction (<800/day), oral NaCl
If symptomatic + Na <110
- IV 500ml NS + 25ml 5.85% NaCl (=100mol NaCl) over 4-6h + IV Lasix 40mg until Serum Na >120
- Then fluid restriction
- Too rapid correction –> Central pontine myelinolysis
21
Q
Causes of SIADH
A
CNS
1. Meningitis, Encephalitis, Brain abscess
2. Head trauma, SAH, CVA, Increase ICP
RS
3. CA Lung
4. Chest infection, positive pressure breathing
Drugs
5. SSRI, Ecstasy
Hypothyroidism
22
Q
S/S of HypoNa
A
Non-specific: Malaise, lethargy, headache
Confusion, convulsion, coma
23
Q
S/S of HyperNa
A
Thirst
Muscle spasm, twitching
Seizure, coma
24
Q
Mx of HyperNa
A
Pure water loss Water deficit = BW x (Na/140 - 1) 1/3 rule in rate of replacement 1/3 in first 8h 1/3 in second 16h 1/3 in third 24h Replace ongoing loss
Too rapid –> Cerebral edema (influx of water into cells due to decreased serum osmolarity)
Max correction rate <12mmol/L/day
25
TTKG
Transtubular K gradient
Tubular [K] / Serum [K]
= (Urine [K] x Serum osmolarity / Urine osmolarity) / Serum [K]
26
HypoK + TTKG >4
Renal loss
| - High [K] in terminal cortical collecting duct
27
S/S of HypoK
Muscle weakness, proximal muscle myopathy
Cardiac arrhythmia (esp <2.0)
ECG: Large U wave, Loss of T wave, Prolong QT interval
Ileus, constipation
Rhabdomyolysis
Polyuria
28
Mx of HypoK
Oral if mild
IV KCl if mod to severe; oral not possible, e.g. Vomiting
Dilute KCl in NS before giving
29
S/S of HyperK
```
Muscle weakness (when >8)
Cardiac arrhythmia (when >6; rate is more important)
ECG
- Peak T
- Widen QRS complex
- Loss of P wave
```
30
Cockcroft-Gault formula
Modified of Diet in Renal Disease (MDRD) equation
RB
Cockcroft-Gault formula
- Plasma creatinine, BW, age, gender
Modification of Diet in Renal Disease (MDRD) equation
- More complex
- Plasma creatinine, serum albumin, BUN, age, gender, race
31
GFR from 24h urine
| RB
UV / P
| Urine Cr x 24h urine volume / Plasma Cr
x1000)/(24*60
32
Long term Cx of CRF
| RB
```
Anemia
Renal bone disease
Bleeding diathesis
Metabolic disturbances
- HyperK
- HypoCa
- Hyperphosphatemia
- Hyperuricemia
- Metabolic acidosis
Malnutrition
CVS morbidities (HT, HL, fluid retention, HF, vascular and valvular calcifications)
Dermatological abnormalities
- Pruritus, skin pigmentation, nail changes
Defective immune responses, susceptible to infection
Menstrual disturbance
Sexual dysfunction
```
33
Reason for Abnormal skin complexion for CRF
| RB
Co-existence of anemia + retention of beta-melanocyte-stimulating hormone, as well as pigment deposition (urochromogens)
34
Indications of Emergency dialysis
| RB
1. HyperK
2. APO
3. Severe metabolic acidosis
4. Uremic pericarditis or Cardiac tamponade
5. Uremic encephalopathy
35
DM nephropathy clinical definition
| RB
?Persistent proteinuria >500mg/24h in a patient with DM with no other renal diseases
36
ANCA
Anti-neutrophil cytoplasmic Ab
| Mainly IgG
37
Tx of IgAN
| RB
Low salt and low protein diet
| ACEI or ARB to block RAAS and reduce BP, reduce proteinuria, provides renal protection
38
Tx for Lupus nephritis
| RB
Corticosteroid (mod to high dose) with gradual tapering
Combined with Cyclophosphamide (IV/PO) for 2-6m
Followed by maintenance with Azathioprine (or MMF)
39
Diagnostic features of peritonitis complicating PD
| RB
- Fever
- Abd pain
- Turbid peritoneal dialysis effluent with WBC >100/mm3
40
Common organisms for peritonitis complicating PD
| RB
```
Gram pos
- Coagulase neg Staphylococcus
- S. aureus
Gram neg
- E coli
M tb
Fungal
```
41
Continue PD while having peritonitis?
| RB
Yes, unless peritonitis refractory to ABX
42
When to initiate RRT
GFR <10 ml/min/1.73m2
or
Symptomatic of uremia
43
Tx for Peritonitis complicating PD
Intraperitoneal
1st gen cephalosporin + Aminoglycoside
(e.g. Cefazolin + Amikacin)
44
Cx of PD
1. Exit site infection
2. PD related peritonitis
3. PD failure
4. PD catheter malposition
5. Peritoneal leakage
45
Cx of HD
Related to vascular access
- Vascular access stenosis / thrombosis
- UL ischemia
Related to catheter access
- Catheter exit site infection
- Catheter associated bacteremia
- Catheter malfunction
During HD
- Hypotension, cardiac arrhythmia
- Muscle cramps
- Technical (should not happen): Air embolism, blood loss
46
Classification of GNs
Primary/Secondary
| Proliferative/Non-proliferative
47
Primary proliferative and non-proliferative GNs
Prim pro
1. IgAN
2. IgMN
3. Membranoproliferative GN
4. Crescenteric GN
Prim non-pro
1. Minimal change disease
2. Membranous nephropathy
3. FSGS
4. Thin basement membrane disease
48
Secondary proliferative and non-proliferative GNs
Secondary pro
1. Lupus nephritis
2. Post-strep GN
3. Hep B/C related membranoproliferative GN
4. Systemic vasculitis
5. Goodpasture syndrome
Secondary non-pro
1. DM nephropathy
2. HT nephrosclerosis
3. Amyloidosis
4. Light/heavy chain deposition disease
5. Alport's syndrome
6. Infection-related membranous glomerulopathy
7. HIV nephropathy (FSGS or collapsing glomerulopathy)
8. Drug-induced glomerulopathy
9. Malignancy-associated nephropathy
10. Reflux nephropathy
49
GN present as 1 of 6 of these clinical syndromes
1. Asymptomatic microscopic hematuria/proteinuria
2. Macroscopic hematuria
3. Acute nephritic syndrome
4. Nephrotic syndrome
5. Rapidly progressive GN
6. Chronic GN / CKD
50
HypoNa pathway
Normal serum osmolarity --> PseudohypoNa due to HL or hyperproteinemia
High serum osmolarity --> Hypergly
Low --> Check urine osmolarity
If Urine Na >20mmol/L
If --> Euvolemia --> (Chronic water overload) --> SIADH, Drugs, CRF, Hypothyroid, Cortisol deficiency
If --> Hypovolemia --> (Renal Na loss) --> Diuretics, Addison's disease, Salt losing nephritis
If Urine Na <20mmol/L
If Hypervolemia --> (Renal Na retention) --> Cirrhosis, HF, Nephrotic syndrome
If Hypovolemia --> (Extra-renal Na loss) --> Vomiting, diarrhea, skin loss
If Euvolemia --> (Acute water overload) --> Increased water intake + Hypovolemia / Drugs / Hypothyroidism / Cortisol deficiency / Renal failure
51
Causes of CKD
1. DM (~45%)
2. HT/Vascular (~10%)
3. Chronic GN (~20%). *common in China, a lot of IgA disease – more aggressive than in the West
4. Chronic pyelonephritis
5. Polycystic kidney disease
6. Drug induced
7. Myeloma, vasculitis, SLE, Alport’s
8. Obstruction
9. Old age
10. Unknown (~15%)
52
NcNc anemia in CKD why?
Lack of EPO
53
S/S of Uremia
| wiki
```
Progressive weakness
Easy fatigue
LOA due to N/V
Muscle atrophy
Tremors
Abnormal mental function
Frequent shallow respiration
Metabolic acidosis
```
54
NSAID AKI mechanism, associations
- Na, fluid retention
- Decrease renal blood flow and GFR
- Leads to HyperK, Tubulointerstitial nephritis, Minimal change disease
- Papillary necrosis in DM
- If Nephrotic syndrome,
- Asso w/ T cell, Eosinophils
- Minimal change disease, Tubulointerstital nephritis
55
CI for Percutaneous renal biopsy
| TC
1. Uncorrectable bleeding diathesis
2. Small kidneys which are generally indicative of chronic irreversible disease
3. Severe HT, which cannot be controlled with antihypertensive
4. Multiple, bilateral cysts or a renal tumor
5. Hydronephrosis
6. Active renal or perirenal infection
7. An uncooperative patient
8. Solitary kidney
56
SE of Cyclosporin A
RB
(Calcineurin inhibitor, decrease IL-2)
1. Immunosuppression
2. Nephrotoxicity (both acute + chronic)
3. HT
4. HL
5. Hypertrichosis
6. Gingival hypertrophy
7. Lymphoma
57
SE of Azathioprine
RB
(Purine analog, Antimetabolite)
(Block de novo purine synthesis)
1. Immunosuppression
2. Myelosuppression (dose-related; caution with Allopurinol)
3. Alopecia
4. Hepatitis
?Lymphoma
58
Sirolimus (aka Rapamycin; mTOR inhibitor)
- A macrolide
- SE
1. HL
2. HT
3. Thrombocytopenia
4. Leukopenia, infection
Interact with Cy A for renal toxicity (and Cy A increases its HL)
59
```
Mycophenolate mofetil (MMF; Antimetabolite)
(inhibits inosine monophosphate dehydrogenase (IMPDH) and suppresses de novo purine synthesis)
```
SE
1. Diarrhea
2. N/V
3. Abd pain
4. Anemia, Leukopenia
60
Tacrolimus (FK 506)
1. Nephrotoxicity
2. Neurotoxicity (tremor, insomnia, and paresthesias of the extremities)
3. New-onset DM
61
Phosphate binders
CaCO3
| Taken with meal to reduce phosphate absorption
62
Amyloidosis Dx
Biopsy (can do fat pad biopsy - biopsy of the SC fat)
Stain with Congo red, combine with Polarized light --> apple green on microscopy
63
Nephritic syndrome
Gross hematuria
Oliguria
HT
Edema
