Renal Flashcards
Nephrotic syndrome key features
- Massive proteinuria (>3.5g/24h or 40mg/hr/m2 for children)
- Hypoalbuminemia (<30g/L)
- Generalized edema
- HL
Nephrotic syndrome PE findings
- Periorbital edmea
- Ankle edema
- Muehrcke’s nails
- Xanthelasma
- Frothy urine
S/S of CKD
- Fatigue
- Nocturia
- Thirst
- Fluid retention
- Itch
Tx target of DM nephropathy
- Control HT, DM, HL
- ACEI for reducing proteinuria
- Anti-inflammatory/fibrosis
Acidosis/Alkalosis on K
Acidosis –> HyperK
Alkalosis –> HypoK
Normal pH / QM ref range
Normal pH: 7.35-7.45
[H] = 40nmol/L @ 7.4pH
Acid/Alkalosis vs Acid/Alkalemia
- osis = a process
- emia = too much/too little H in blood
Metabolic acidosis features
Decreased HCO3 (Normal: 22-28mmol/L) Hyperventilation to compensate
Dx of Metabolic acidosis
Determine Anion gap
If high –> Done
If normal –> determine Urine anion gap
Look for any osmolar gap
Normal value Anion gap
8-14
[Na - Cl - HCO3]
If normal AG –> Cl is increased
Metabolic acidosis with increased AG
Causes
- DKA
- Alcoholic KA
- Lactic acidosis
- Renal failure
- Rhabdomyolysis
Metabolic acidosis with normal AG
Causes
- 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)
Osmolar gap (OG) How to calculate
Actual - Calculated plasma osmolarity
Calculated = 2xNa + Urea + Glucose
Increased = Something osmolar inside, e.g. alcohol related compounds)
Lactic acidosis type A and B
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
Risk of NaHCO3 therapy
- 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)
RTA (Renal tubular acidosis) types and features
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
Mx of RTA
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
Causes of Metabolic alkalosis
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)
Tx of Metabolic alkalosis
If ECF contracted –> Give Saline (HCO3 will fall with expansion)
IF ECF expanded –> IV HCl or Oral NH4Cl to correct alkalosis
Correct HypoK
SIADH
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
Causes of SIADH
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
S/S of HypoNa
Non-specific: Malaise, lethargy, headache
Confusion, convulsion, coma
S/S of HyperNa
Thirst
Muscle spasm, twitching
Seizure, coma
Mx of HyperNa
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
TTKG
Transtubular K gradient
Tubular [K] / Serum [K]
= (Urine [K] x Serum osmolarity / Urine osmolarity) / Serum [K]
HypoK + TTKG >4
Renal loss
- High [K] in terminal cortical collecting duct
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
Mx of HypoK
Oral if mild
IV KCl if mod to severe; oral not possible, e.g. Vomiting
Dilute KCl in NS before giving
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
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
GFR from 24h urine
RB
UV / P
Urine Cr x 24h urine volume / Plasma Cr
x1000)/(24*60
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
Reason for Abnormal skin complexion for CRF
RB
Co-existence of anemia + retention of beta-melanocyte-stimulating hormone, as well as pigment deposition (urochromogens)
Indications of Emergency dialysis
RB
- HyperK
- APO
- Severe metabolic acidosis
- Uremic pericarditis or Cardiac tamponade
- Uremic encephalopathy
DM nephropathy clinical definition
RB
?Persistent proteinuria >500mg/24h in a patient with DM with no other renal diseases
ANCA
Anti-neutrophil cytoplasmic Ab
Mainly IgG
Tx of IgAN
RB
Low salt and low protein diet
ACEI or ARB to block RAAS and reduce BP, reduce proteinuria, provides renal protection
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)
Diagnostic features of peritonitis complicating PD
RB
- Fever
- Abd pain
- Turbid peritoneal dialysis effluent with WBC >100/mm3
Common organisms for peritonitis complicating PD
RB
Gram pos - Coagulase neg Staphylococcus - S. aureus Gram neg - E coli M tb Fungal
Continue PD while having peritonitis?
RB
Yes, unless peritonitis refractory to ABX
When to initiate RRT
GFR <10 ml/min/1.73m2
or
Symptomatic of uremia
Tx for Peritonitis complicating PD
Intraperitoneal
1st gen cephalosporin + Aminoglycoside
(e.g. Cefazolin + Amikacin)
Cx of PD
- Exit site infection
- PD related peritonitis
- PD failure
- PD catheter malposition
- Peritoneal leakage
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
Classification of GNs
Primary/Secondary
Proliferative/Non-proliferative
Primary proliferative and non-proliferative GNs
Prim pro
- IgAN
- IgMN
- Membranoproliferative GN
- Crescenteric GN
Prim non-pro
- Minimal change disease
- Membranous nephropathy
- FSGS
- Thin basement membrane disease
Secondary proliferative and non-proliferative GNs
Secondary pro
- Lupus nephritis
- Post-strep GN
- Hep B/C related membranoproliferative GN
- Systemic vasculitis
- Goodpasture syndrome
Secondary non-pro
- DM nephropathy
- HT nephrosclerosis
- Amyloidosis
- Light/heavy chain deposition disease
- Alport’s syndrome
- Infection-related membranous glomerulopathy
- HIV nephropathy (FSGS or collapsing glomerulopathy)
- Drug-induced glomerulopathy
- Malignancy-associated nephropathy
- Reflux nephropathy
GN present as 1 of 6 of these clinical syndromes
- Asymptomatic microscopic hematuria/proteinuria
- Macroscopic hematuria
- Acute nephritic syndrome
- Nephrotic syndrome
- Rapidly progressive GN
- Chronic GN / CKD
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
Causes of CKD
- DM (~45%)
- HT/Vascular (~10%)
- Chronic GN (~20%). *common in China, a lot of IgA disease – more aggressive than in the West
- Chronic pyelonephritis
- Polycystic kidney disease
- Drug induced
- Myeloma, vasculitis, SLE, Alport’s
- Obstruction
- Old age
- Unknown (~15%)
NcNc anemia in CKD why?
Lack of EPO
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
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
CI for Percutaneous renal biopsy
TC
- Uncorrectable bleeding diathesis
- Small kidneys which are generally indicative of chronic irreversible disease
- Severe HT, which cannot be controlled with antihypertensive
- Multiple, bilateral cysts or a renal tumor
- Hydronephrosis
- Active renal or perirenal infection
- An uncooperative patient
- Solitary kidney
SE of Cyclosporin A
RB
(Calcineurin inhibitor, decrease IL-2)
- Immunosuppression
- Nephrotoxicity (both acute + chronic)
- HT
- HL
- Hypertrichosis
- Gingival hypertrophy
- Lymphoma
SE of Azathioprine
RB
(Purine analog, Antimetabolite)
(Block de novo purine synthesis)
- Immunosuppression
- Myelosuppression (dose-related; caution with Allopurinol)
- Alopecia
- Hepatitis
?Lymphoma
Sirolimus (aka Rapamycin; mTOR inhibitor)
- A macrolide
- SE
- HL
- HT
- Thrombocytopenia
- Leukopenia, infection
Interact with Cy A for renal toxicity (and Cy A increases its HL)
Mycophenolate mofetil (MMF; Antimetabolite) (inhibits inosine monophosphate dehydrogenase (IMPDH) and suppresses de novo purine synthesis)
SE
- Diarrhea
- N/V
- Abd pain
- Anemia, Leukopenia
Tacrolimus (FK 506)
- Nephrotoxicity
- Neurotoxicity (tremor, insomnia, and paresthesias of the extremities)
- New-onset DM
Phosphate binders
CaCO3
Taken with meal to reduce phosphate absorption
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
Nephritic syndrome
Gross hematuria
Oliguria
HT
Edema