Nephrology Flashcards
Acid/Bases Review
pH >7.4
HCO3 is UP
PCO2 normal or UP
= METABOLIC alkalosis
PCO2 is DOWN
HCO3 normal or down
= RESPIRATORY alkalosis
pH<7.4
PCO2 is up
=Respiratory
acidosis
HCO3 is down
= metabolic
acidosis
- Compensation?
-Metabolic Acidosis 1:~1 (↓ HCO3 :↓ CO2) *winter’s formula/last 2 digits of pH ± 2
-Metabolic Alkalosis 1:0.7 (↑ HCO3 : ↑ CO2)
-Respiratory Alkalosis (↓ CO2 : ↓ HCO3). Chronic (10:4-5) / Acute (10:2)
-Respiratory Acidosis (↑ CO2 : ↑ HCO3). Chronic (10: 3-4)/ Acute (10:1)
Metabolic Acidosis- calculations
- Calculate the anion gap: Na – Cl – HCO3
– Adjust for albumin (every decrease in albumin by 10, add 2.5mEq/L to
the AG) - Calculate the “delta-delta”: ΔAG (12-AG):Δbicarb(24-bicarb)
– The delta AG (from normal = 12) should be equal to the change in
bicarb (from normal = 24) when pure AGMA
– See next slide - Calculate the osmol gap: [calculated osm: 2xNa + Gluc + BUN] –
[serum measured osm]
– Normal osmolar gap = 10; higher means additional unmeasured
osmoles− think EtOH or toxic alcohol (dangerous to miss!)
– Could have high osmolar gap with normal anion gap early in toxic alcohol
Delta:Delta
∆AG»_space;∆HCO3 >2, bicarb doesn’t change enough, meaning a secondary alkalosis is opposing the acidosis.
Concurrent Metabolic alkalosis (HCO3 higher than expected) with anion gap metabolic acidosis.
∆HCO3 ≈ ∆AG 0.8-2, Pure AG acidosis
∆AG «_space;∆HCO3 <0.8, Bicarb changes more than expected, meaning a secondary acidosis is present
Concurrent non AG metabolic acidosis (with HCO3 lower than expected) with high AG acidosis
Causes of AGMA (GOLDMARK)
G- Glycols
O- Oxoproline*
L- Lactate
D- D-lactate
M- Methanol
A- ASA
R- Renal failure
K- Ketones
Causes of Increased Osmolar Gap
Anion Gap Metabolic Acidosis-
Organic alcohol poisoning:
* Methanol
* Ethylene glycol (antifreeze)
Paraldehyde
Ketoacidosis (Etoh + Diabetic)
Lactic acidosis
Severe CKD
No Metabolic Acidosis
Ethanol
Isopropyl alcohol (rubbing ETOH)
Mannitol
Sorbitol
*pseudohyponatremia
*Early toxic alcohol!
Acid/Base Disorder Pearls
In organic alcohol intoxications, the osmolar gap and anion gap
may exist at different times
– Early on: osmolar gap without anion gap
– Later: anion gap without osmolar gap
If you see an ABG with pH 7.4, be alert for mixed disorders
– E.g. if the bicarb is low, go through all of the steps for metabolic acidosis
NAGMA Approach
Is NH4 excretion high, as
expected if kidney
working appropriately
Yes
(UAG «0)
-GI HCO3 loss (diarrhea)
Pancreatic fistula
NJ tube
No
(UAG >0) = RTA
Check urinary anion gap:
Urine(Na+) + Urine(K+) – Urine(Cl)
Urine anion gap: If its Negative its
Not the kidney!
NEGUTIVE = the gut
Causes of metabolic alkalosis
Urine Cl < 25: (will be Chloride/NS responsive)
– GI loss (NG tube, vomiting, villous adenoma, chloride diarrhea)
– Renal loss (diuretics)
– Sweating (Cystic fibrosis)
Urine Cl >25: (will not be chloride/NS responsive)
– High BP:
* Hyperaldosterone (htn, hypoK, alkalosis, high aldo)
* Liddle’s (htn, hypoK, alkalosis, low aldo)
* Cushings
– Low BP:
* Barter’s (mimics Loops – low K, low Mg)
* Gittleman’s (mimics thiazides – low K, low Na, high Ca)
– Excess bicarb ingestion
Hyponatremia- correction calculation
The most important questions to answer on initial assessment:
– Is this a medical emergency?
– Is this symptomatic or asymptomatic?
– Is this acute, chronic, or acute-on-chronic?
* Acute <48hrs
Hyponatremia correction formula:
– Volume infusate to give = TBW x (desired Na – Serum Na)/ [Na] infusate
– Infusate = solution you choose to give
* Hypertonic saline 3%- 513mmol/L Na
* Normal Saline 0.9% - 154mmol/L Na
* Ringers Lactate- 130mmol/L Na
TBW= Total Body Water
Female- 50% of Wt (Kg) or Wt (Kg) x 0.5
Hyponatremia: Severe Symptoms
Severe and symptomatic (usually also acute).
* (ie) 60 kg woman presenting with seizures, Na of 110.
– Goal: increase serum Na by 4-5 mmol/L immediately
– Volume infusate to give = TBW x (desired Na – Serum Na)
[Na] infusate
* = (60kg x0.5) x (115 – 110)
513
* = 0.292L ~ 300mL
– Therefore, give ~300cc of 3% saline to raise this patient’s serum Na by
5mmol/L
Non-acute hyponatremia
- If not symptomatic/acuteà there is time
- Hypertonic saline usually not needed (some exceptions likely not for the
scope of this exam)
Obtain Uosm, S osm, Una
* Stop thiazides
* Thorough history (medications, diet, fluid intake, volume status)
While waiting for tests:
* If they are hypotensive -> bolus and repeat levels
* If they are hypovolemic -> 1ml/kg/hr
Hyponatremia Etiology
- Hyponatremia is a problem of too much water in the body
Too much water comes from
1. Too much water intake compared to salt
– Psychogenic polydipsia, beer potomania, D5W
– ADH off – pee out excess water –dilutes urine –low urine osm (<200)
High Water:Solute intake
* ADH is appropriately off (U osm <200)
- Causes
– psychogenic polydipsia- urine osm typically <100
– Beer potomania/tea and toaster: low solute diet –Urine osm ~100-300 - If you only eat 200 mOsmol/day and can only dilute urine to 100
mOsmol/L, max UO = 2L/d. Drink more than 2L/day, and you will retain
free water and drop Na
– Iatrogenic: eg IV D5 ++
– Treatment: Fluid restrict, salt/urea tabs (increases solute load AND will
increase water diuresis)
- Reabsorption from urine (ADH mediated) – ADH on –reabsorb water from urine –concentrate urine + dilutes the serum – high urine osm (>300) + hyponatremia
– ADH is on because of appropriate and inappropriate reasons
Inappropriate ADH secretion (U osm >300, Una>40)
1. SIADH
* Nausea/vomiting, Pain, Drugs- TCAs, SSRIs, carbamazepine, ecstasy/MDMA, Thiazides, CNS disorders, tumors (SCC
lung), Pneumonia/ lung infections, adrenal insufficiency, hypoT4
– Treatment: fluid restriction (next step is to add salt tablets 1 g BID/TID and/or urea 15 mmol BID)
Appropriate ADH secretion (U osm >300, Una<25):
1. True hypovolemia
– Causes: burns, bleeds, GI losses, pancreatitis
– Treatment = fluid resuscitation (NS/LR) (1ml/kg/hr)
2. Decreased effective circulating volume
– Causes: CHF, cirrhosis, hypoalbuminemia
– Treatment: Optimize underlying condition, Furosemide, Water restriction
Over-Correction of Hyopnatremia
Tip: “If urine output exceeds 150 ml/hr page MD”
– Indicates that ADH has turned off and patient will suddenly start
peeing free water thus raising serum sodium faster than
expected
– IF overcorrected:
– DDAVP
– D5W
– Call nephro
targret 6-8mmol/L per 24 hours
(4-6 if risk factors)
Hyponatremia pearls
Isotonic hyponatremia (sOsm 280-295): Pseudohyponatremia -hypertriglyeridemia
-paraproteinemia (multiple myeloma)
-obstructive jaundice
Hypertonic (sOsm >295) hyponatremia -hyperglycemia
-mannitol
-Immunoglobulins (IVIG)
Hyponatremia in the dialysis population: they’re drinking too much water
inbetween sessions! Treatment : fluid restriction (not salt restriction)
Management of Hypernatremia
Dehydration or Free Water Deficit
1. Calculate Water Deficit= % change in [Na] x TBW
– Where % change in [Na] = Serum Na- 140
140
- Determine rate of correction of water deficit:
– Acute (e.g. postop central DI, nephrogenic DI): Correct quickly (rare)
– Chronic (e.g. dementia LTC patients): Correct water deficit slowly: maximum 0.5 mmol/L
per hour/ 12 points over 24 hours (Avoid cerebral edema!)
* IF POSSIBLE USE ENTERAL ROUTE (If NG, give free water flushes)
* Large volumes of D5 –>hyperglycemia –> glucosuria & a solute diuresis, worsening polyuria and
hypernatremia
Diabetes Insipidus (DI)
Clinical clues: polyuria + hypernatremia
– (and polydipsia if patient is able to drink)
* Types of DI:
– Central DI (brain can’t make/secrete ADH)
– Nephrogenic DI (kidney can’t respond to ADH)
– causes: Lithium, hypercalcemia, hereditary, resolution of obstructive nephropathy
Diagnosis:
– Step 1: One of:
* Labs: high serum Na with inappropriately low urine osmolality confirms diagnosis
* Water deprivation test: Urine osmolality does not rise appropriately despite
rising serum osmolality/ serum Na
– Step 2: DDAVP (2-4 mg IV/SC) test to differentiate between central and nephrogenic DI
Hyperkalemia- Causes
Increased intake – unlikely to be sole cause
Decreased excretion
– Decreased tubular flow: CKD, Volume depletion – Drugs- ACEi/ARB, NSAIDs, MRAs
-Hypoaldosteronism: adrenal insufficiency, RTA type 4
* Shifting
– Cell lysis- TLS, Rhabdo, burns
– Metabolic- Acidosis, low insulin
– Hyperosmolarity: glucose, mannitol
– Familial hyperkalemic periodic paralysis
*
Factitious
– Fist clenching/ tourniquet – Hypercellular blood ( ie- heme malignancies)
* High WBCs, thrombocytosis * Do a VBG/ABG! – no tourniquet and no centrifuge
= no hemolysis in tube
– Hemolyzed sample
Treatment of Hyperkalemia
Treat hyperkalemia with C-BIG K:
C- calcium gluconate 1g IV – stabilize the heart
B- beta agonist (Ventolin)/ Bicarbonate
I-insulin (10 units insulin R IV)
G- glucose (1 amp D50 BEFORE insulin)
K- K removal: Furosemide/K binders/ dialysis
Potassium Binders
1) Lokelma/ sodium zirconium cyclosilicate (ZS-9) * Exchanges Na and H+ for K in the GI tract
– See drop in K within 2-4 hours of administration
* Safety shown in patients with CKD, can be used long term to facilitate continued RAAS
blockade (HARMONIZE trial)
* Safety shown in IHD patients with chronic pre-HD hyperkalemia (DIALYZE study)
* Side effects- edema, GI symptoms,
* $$$ a barrier, off formulary typically
2) Patiromer: binds K in the colon, in exchange for Calcium
3) Kayexalate (Polystyrene sulfonates)
- exchange Na+ in stomach for H+, which is then exchanged in colon for K+ and resin
is excreted
- Caution if GI obstruction, risk of hypoCa and hypoMg also
- Associated with cases of colonic necrosis, bleeding, ischemic colitis, perforation
Hypokalemia- causes
- Decreased intake
- Check Serum Mg!
- Shifting (usually causes acute hypokalemia)
– Endocrine causes
* ++Insulin, thyrotoxic periodic paralysis
– Stress: ++ catecholamines
– Acid/base- Metabolic alkalosis
– Alcohol withdrawal
– Hypothermia
– Drugs
* Amphetamines, antipsychotics (rare)
Chronic hypokalemia: K loss
Step 1: Check urine lytes
Extra renal: Low urine K < 20*
I.E. Diarrhea, laxatives, villous adenoma
*In real life look at Urine K: creat ratio
(<2 with extra renal loss, > 2 renal)
Renal Loss (Urine K> 20)
Step 2: acidosis vs. alkalosis
-Met Acidosis- Type 1 or 2 RTA
Met Alkalosis- Step 3
Hypertensive vs.
Normo/ hypotensive
Hypertension- Low Renin/ Low Aldo:
e.g. Cushings, Liddles,
Licorice, Florinef,
steroids
High Renin/ high Aldo:
e.g. RAS/Reninoma
Low Renin/ high Aldo:
Adrenal problem
e.g. Conns
Normo/ Hypotensive:
Urine Chloride-
Urine Cl <20:
Vomiting or intermittent
diuretic use ( already
“worn off”)
Urine Cl > 20: Barrter.
Gitelman
or recent diuretic use
HTN- first line therapy
Long-acting thiazide (chlorthalidone)/thiazide-like diuretics preferred over
hydrochlorothiazide (HCTZ)
– Watch for hypoK + hypoNa if using thiazide monotherapy
* ACEi monotherapy
– Do not use in Black patients without other indications
– Not first line in isolated systolic hypertension
* ARB
* Long-acting CCB
* β-blockers can be considered first line only if <60 years old
– Do not use alpha-blocker first line
BP Targets – CKD
CKD Target: Hypertension Canada 2020, C-CHANGE 2022
“Individualize BP targets in patients with CKD.”
- CKD patients who meet high risk (SPRINT) criteria, target SBP< 120, in Diabetics: <130/80
- In Polycystic Kidney Disease target SBP <110 if meets certain criteria – more in bonus slides
KDIGO 2021 CKD and HTN guideline:
– Target SBP <120, up titrate ACE/ARB as high as tolerated [Gr2B]
* In all CKD = Diabetic and non-Diabetic (*not dialysis/post transplant)
– SBP <120 is recommended with greater certainty among patients at higher risk for CV disease
(AKA SPRINT CANDIDATES)
– With less certainty among patients with diabetes, stage 4 or 5 CKD, severe albuminuria (ACR
>300 mg/g), prior stroke, very low diastolic BP, and severe hypertension
» BASICALLY Less Certaintin for tHE Patients EXCLUDED FROM SPRINT
– Post transplant: long term <130/80, use DHP-CCB or ARB first line
Hyperaldosteronism: – Who to Screen: Patients with hypertension AND 1 or more:
- Unexplained spontaneous hypokalemia <3.5 or marked diuretic related hypokalemia <3.0
- Htn & resistant to treatment with ≥ 3 drugs
- Incidental adrenal adenoma AND Htn
How to Screen
* Plasma aldosterone and plasma renin activity or plasma renin concentration
* Do not use plasma renin conc. In women on OCP (false +)
* Drugs that interfere (MRAs > ACEi/ARB»_space; BB, CCB)
* Hold MRA, K sparing and K wasting diuretics at least 4 weeks prior to testing
* If result non diagnostic, hold ACE/ARB, BB, DHP-CCB 2 weeks and repeat testing
* BP meds that do not interfere: alpha blockers, non DHP CCBs, hydralazine
– If screening test positive do confirmatory test with:
* Saline loading test (2L NS over 4h, measure plasma aldo afterward, abN if >280 pmol/L
* Captopril suppression test
* Plasma aldosterone to renin ratio > 1400 pmol/L/ng/mL/h (or > 270 pmol/L/ng/L), with plasma
aldosterone > 440 pmol/L ((HTN 2020)
Renovascular HTN- who to screen and How
Who to screen
– Patients presenting with 2 or more of the following
* Sudden onset or worsening HTN age >55 or <30
* Abdominal bruit
* HTN resistant to ≥ 3 drugs
* Increase in Cr ≥ 30% with ACEi or ARB
* Other atherosclerotic vascular disease, particularly in smokers or dyslipidemia
* Recurrent pulm edema associated w/ Hypertension emergency
- How to Screen
– Any of: Renal Doppler US, captopril renogram, MRA, CTA - Avoid captopril and CTA if renal GFR <60 ml/min/1.73m2
ACEi or ARB not contraindicated with bilateral renal artery stenosis
Atherosclerotic RAS is managed medically
– no benefit to stenting over medical therapy in most
* Angioplasty and stenting could be considered if any of the following present:
(REVISED in 2020 guidelines)
1. uncontrolled HTN resistant to maximally tolerated pharmacotherapy
2. progressive renal function decline
3. Acute pulmonary edema
Pheochromocytoma – Who to Screen and How to screen
Paroxysmal, unexplained, labile, and/or severe (≥ 180/110) sustained HTN refractory to usual
therapy
– HTN + symptoms of catecholamine excess (headaches, palpitations, sweating, flushing)
– HTN triggered by beta-blockers, MAO-Is, surgery, anesthesia, micturition
– Incidental adrenal adenoma
– Hereditary causes– such as Von-Hippel-Lindau, MEN 2A or 2B, neurofibomatosis type 1
How to Screen
– Biochemical screening test first
– YES ✓ – 24hr urine total metanephrines and catecholamines (and Creatinine to ensure
adequate collection)
– MAYBE – Plasma free metanephrines and free normetanephrines may also be considered
– NOT ❌ urinary VMA
