Renal Flashcards
Type II RTA
Proximal
Defect in bicarbonate reabsorption, usually associated with features of Faconi syndrome, including glycosuria, aminoaciduria, phosphaturia, and uriscoruria(indicating PT dysfunction)
What causes isolated proximal RTA(type II)
Hereditary dysfunction of the basolateral sodium-bicarbonate cotransporter.
Faconi may be inherited or acquired due to myeloma, chronic IN, or drugs (tenofovir, ifofamide)
Treat proximal RTA ((type II)
Large doses of bicarbonate which may aggravate hypokalemia
Type IV RTA
May be due to hyporeninemic hypoaldosteronism or to resistance of the distal nephron to aldosterone.
Hyporeninemic hypoaldosteronism is typically associated with volume expansion nand most commonly seen in elderly and/diabetic patients with CKD
Hyperkalemia associated with NSAIDS and cyclosporine
Partially due to hyporeninemic hypoaldosteronism
Patients with hyporeninemic hypoaldosteronism are typically __kalemic; they may also exhibit ___ acidosis, with urine ph<5.5 and a ___ urinary ion gap
Hyper
Mild non anion gap
Positive
In type IV, acidosis often improves with reduction in serum _ (treatment)
K
Hyperkalemia appears to interfere with medullary concentration of ammonium by the renal countercurrent mechanism
How treat type IV if acidosis doesn’t improve with reduction of K
Oral bicarbonate or citrate
Type IV and various forms of distal tubular injury and tubulointerstitial disease (interstitial nephritis)
Associated with distal insensitivity to aldosterone; urine pH is classically >5.5, again with a positive urinary anion gap
Definition of urinary tract infection
Encompasses a variety of clinical entities: cystitis, pyelonephritis, prostatis, asymptomatic bacteriuria
Uncomplicated UTI
Acute disease in non pregnant outpatient women
Without an atomic abnormalities or instrumentation of the urinary tract; ____ ___ refers to all other types of UTI
Complicated UTI
Calculate and interpret anion gap in an acid/base disorder
Interpret blood gas and correctly name the acid/base disorder
Identify compensatory mechanisms for metabolic acidosis
Identify the most common causes of high anion gap metabolic acidossi
Know
Henderson hasselbalch equation
Bicarbonate and pCO2 are the drivers of pH
Acidemia
<7.35
Alkalemia
> 7.45
Acidemia metabolic acidosis or respiratory acidosis
Metabolic
HCO3<20
Respiratory
PCO2>45
Alkalemia metabolic or respiratory
Metabolic
HCO3>30
Respiratory alkalosis pCO2<35
Increased endogenous acids
Ketoacidosis Lactic acidosis -diabetic -alcoholic -starvation
Increased ingestion of acids
Ethylene glycol
Methanol
Propylene glycol
Salicylate
Loss of bicarbonate
Diarrhea
Decreased secretion of acids
AKI
-defined by serum Cr
Chronic kidney disease
-defined as increase in GFR
Signs and symptoms of acidosis
Headaches
Ab pain
Malaise
“I have the flu”
Change in mental status-confusion, stupor, coma
Increased respiration’s
Variable changes in bp
Tachycardia-catecholamie release
Pulmonary need,s-changes in pulmonary compliance
Increased serum glucose-this is reactive be careful
Anion gap
Na-(Cl+HCO3)
BMP
Na K Bicarb CO2(when see CO2 it means bicarbonate)
Normal anion gap is 10, why positive
Albumin is primary unmeasured anion
* there are unmeasured anions!!!!!!
Total cations
Measured cations MC and unmeasured cations UC
Total anions
Measured anions MA and unmeasured anions (UA)
Normally MC+UC=MA+UA_> (Na+K)-(Cl+HCO3)
(MC+UC)-MA)=UA
Anion gap is a way of demonstrating accumulation of the __
UA
Elevation of anion gap suggests what
Metabolic acidosis itch circulating anion
Compensation
Respiration goes up under stress bc CO2 is very easy to blow off. It’s an immediate response
Respiratory changes take minutes
Metabolic take longer
So start blowing off CO2 with acidosis
Sometimes body will blow off so much CO2 that what happens
Get respiratory alkalosis-use equation for compensation
PCO2=(1.5xHCO3)+8(+/-2)
If calculated doesn’t match, then there is a respiratory alkalosis
Compensation always exists
However it will not completely reserve the primary problem. It is the normal physiologic response to attenuate the problem
Compensation can be appropriate, inadequate, or excessive
MUD PILES- most common causes of anion gap increase
Methanol, metformin
-wood alcohol-solvent
Uremia->renal failure
Diabetic ketoacidosis (type I, also includes starvation ketoacidosis
Paraldehyde, propylene glycol, phenformin
Isoniazid/iron toxicity
Lactic acidosis
->includes cyanide and CO poisoning, seizures, sepsis, ischemia
Ethanol/ethylene glycol
Salicylate
Glue a pain huffing?
Toluene first high anion gap then low! Weird acidosis picture
A 72 yo male presents with acute illness and leg pain. He sustained a cut on his lef while working in the years 10 days ago. Over 3 days, pain increased. He has fever, chills, nausea, and vomiting. He has only been able to tolerate small amounts of quirked over 24 hours he has not urinated for 12 hours.
BP 90/60, HR 125, RR 24, T 101.3
WBC up
Cloudy urine with pH 5.5, specific gravity 1.01
Casts muddy brown-tubular necrosis **-THIS IS WY GET URINE MICROSPY
PH 7.5, PCO2 30, CO2 15
BUN:Cr-prerenal?
Acid or base?
Why is Na high-Na not being reabsorbed have tubular dysfunction
1.01—-same concentration as serum, NOT CONCENTRATED!!! Something wrong with kidney
We would expect to be super concentrated
7.35 is normal—-compensation!!! Did you calculate PCO2?
Prerenal azotemia
High anion gap Metabolic acidosis, appropriately compensated (pH and pCO2 nearly the same-usually sign for scompensated but doesn’t always work use
Most likely cause high anion gap metabolic acidosis
Lactate acidosis with
Does this patient need an IV
BUN Cr up tachycardia and hypotensive
Hydrate!
Normal saline bc isotonic want it to stay intravascular -we need to support his cardiovascular status
Why does this patient have nausea and vomiting
Acidosis causes nausea as a compensatory mechanism for acidosis
Every patient it’s acidosis will say they have what
Flu, nausea
Uremia toxicity
80-100 BUN get symptoms
Sepsis presentation
Acute fever, ill, tachycardia, hypotension
Multiorgan involvement in infection removed from the source!! (Wound on leg causes enough problems that get tachycardia, renal failur,e GI distress…)
Hypofunction of uninflected organs
Postulated that there is both overproduction of pyruvate and an inhibition of PDH activity (which you will recall. Is the rate limiting state in oxidative phosphorylation)
What labs
Wound culture ?
Rhabdomyolysis
Event that causes release of intracellular contents into extracellular space
Msucle aches-> hypotension and renal failure
Muscle fiber exhaustion
-seizure, extreme exercise, heat stroke, malignant hyperthermia
Physical injury
-trauma, crush injury, immobilization, compartment syndrome
Drugs , supplements cause rhabdomyolysis
Statins
Selective serotonin reuptake inhibitors
Colchicine
Cocaine
Amphetamines
Heroin
Creatinine
Ephedra
Toxins cause rhabdomyolysis
Alcohol
Toluene
CO
Other causes of rhabdomyolysis
Hypokalemia, hypophosphatemia, excessive fluid shifts, vasculitis, ***influenza, dermatomyositis, polymyositis
Diagnosis rhabdomyolysis HISTORRRRRY
Start with a complete history
Decreased urine output
Reddish brown color d/t presence of myoglobin
Dipstick: heme+but no rbc identified on microscopy +/- protein
Microscopy:granular casts
Serum labs: elevated creatine kinase, hyperkalemia, hypocalcemia, hyperphosphatemia
Acid/base disorder caused by release of lactate and other organic acids
Diabetic ketoacidosis
Have typical symptoms of polyuria and polydipsia
Polyuria: osmotic diuresis due to high serum glucose->dehydration drives thirst (peeing all this stuff out and getting dehydrated which drives thirst…have intracellular hypoglycemia)
Ketones are rapidly excreted int he urine which also helps to maintain GFR and kidney perfusion
Abdominal pain and nausea are driven by acidosis
Vomiting drives a metabolic alkalosis (compensatory mechanism)
Vomiting expels H from gastric contents (which increases HCO3
Ketones are rapidly filtered in place of Cl
***differentiate polyuria from frequency!!!(high volume and a lot with polyuria, frequency just have to go a lot)
Type I diabetic ketoacidosis
Intracellular hypoglycemia which activated FA degranulation which leads t large amounts of ketones
Other : hyperkalemia and rhabdomyolysis
Treat with hydration it will wash out probably just intracellular falling out since membrane issue
Early diabetic
Normal anion gap
As fluid decrease have high anion gap
22 yo type I diabetic doesn’t check insulin but knows when they need it. Ow N/V and ab pain. This is early , vitals ok a bit of tachycardia
Na low PH 7.3 CO2/bicarb-low Glucose-HIGH BUN-high Cr-high end of Normal(prerenal bc diuresed.tachycardic bc now hypovolemia) Ketone +
High K
How treat
HYDATE and insulin (tons-don’t stop insulin)
K goes down (was pseudo)
K and potassium goes back into cells and end up hypokalemic so need to replace after a few hours
Alcoholic ketoacidosis
Stop eating during drinking binges or when vomiting begins
Alcohol levels are negligible upon presentation
Degradation of alcohol depletes NAD which curtails hepatic gluconeogenesis which leads to depletion of liver stores of glycogen
Metabolism of increases the NADH/NAD ration, favoring the conversion of pyruvate to lactate
Similar to DKA in that binge drinking leads to low insulin levels
Dehydration secondary to ADH suppression by etoh complicated by lack of intake but not as severe as DKA
Lactic acid builds up due to impaired hepatic conversion of lactate to glucose
58 yo male ab pain
Low BMO alcoholic
Elevated glucose (not enough for DKA, this isn’t stress response 142 vs 475)
Creatinine up
Ketones positive
N/V
Anion gap-24 (not as high at ketoacidosis)
Normal anion gap 10, this one is 24 so delta gap is 14
Bicarb delta is 8,
14>8 mixed metabolic acidosis
Delta gap 24-14
Ok
Ethylene glycol
Sweet liquor foun in anti freez
100 ml can be fatal
Ethylene glycol is metabolized by alchol DH->glycolic acid->oxalis acid
Increased NADG levels encourage lactic acid formation ‘
Presented with intoxication, low blood alcohol level, and HAGMA without ketones
Calcium oxalate crystals in urine
Fluorescence under wood lamp
Methanol
Found in solvents or impurity in alcoholic beverages
Less intoxication than either ethanol or ethylene glycol
30 ml can be fatal
Metabolized by alcohol DH->formaldehyde-> formic acid which causes MAGMA
NAD depletion favors lactate production
Blurry vision is characteristic or methanol ingestion
Salicylate toxicity (tinnitus and tachypnea)
Presents with tachypnea as salicylate as a direct respiratoy stimulant
Tinnitus is present when serum salicylic acid levels reach 20-45 mg/sL
CNS manifestations: agitation, seizures, coma
Peak serum concentrations: 4-6 hours after ingestion
Tachypnea induces a respiratory alkalosis
Metabolic acidosis is the result of the acccumulation of both lactic acid and ketoacids
Salicylic acid contributes very little of the acid load
Acute renal injury or disease
Staged according to the rate of rise in serum creatinine
Chronic kidney disease
Uses GFR to define and stage CKD
Renal failure
Decreased number of nephrons in CKD leads to:
Decreased ammoniagenesis int he proximal tubule
Result of decreased GFR(90 normal)
- inability to secrete the daily production of fixed acids
- decreased ability to filter and excrete various anions
- accumulation of sulfate, phosphate and othe anions produce anion gap (AG)
-Harrison questions look at them !
Ok
Ok
62 yo man acute confusion . Can’t give history
Smells like alcohol
95/96
HR 96
RR18
Temp 97
PH 7.32
PCO2 30
CO2 low
Acidosis
Low bicarb
Metabolic acidosis
What’s the differential for metabolic acidosis MUDPILES
High anion gap
- uremia? (Look at BUN-get those symptoms at 100)
- DKA-no glucose is normal
- salicylate toxicity-tachypnic no
- CO poisoning-he was outside in parking lot so not if in garage in car.
- methanol, ethanol, lactic acidosis, ethylene glycol
-lets get serum alcoho,, look at urine (black light look for calcium oxalate crystals-ethylene glycol, and fluorescents under black light)
Non anion gap metabolic acidosis is by definition hyper-chloremic acidosis
DKA-high anion gap
Loss of alkali (bicarb) can be from the GI tract or kidneys
Reciprocal changes in Cl and bicarb result in a normal AG
Pure non AG acidosis: increases in Cl equals the decrease in HCO3
There is a change in the transport system that causes acidosis
Can be genetic or acquired
Transport systems have changes
*generalized tubular defect with obstruction
Distal RTA
Type 1
Type II
Bicarb transport change
Type IV
Hypoaldosteronism
Type I
Classic distal RTA
Hypokalemia, positive UAG, pH>5.5
Type II
Proximal RTA
Faconi
Glycosuria, generalized aminoaciduria
Type IV
Distal RTA
Hyperkalemia, positive UAG
Classic distal type I
Inability of the distal tubule to acidity the urine
Familiala : defective HCO3/Cl exchanger and H ATPase
Associated with autoimmune disorders: SLE , Sjorgen syndrome, cryoglobinemia
Drugs: lithium, toluene, amphotericin
RTA type I
Inability to secrete H leads to decreased NH4 in the tubules
Less NH4-> high urin pH>5.5
Positive UAG
Serum hypokalemia (augmented K secretion in lieu of H in exchange for Na reabsorption
Calcium oxalate crystals, osteomalacia, osteoporosis
Patients have hypocitraturia and hypercalciuria so they are prone to nephrolithiasis, nephrocalcinosis and bone disease
Type IV
Hyperkalemia and metabolic acidosis
Asymptomatic with mild hyperkalemia and decreased bicarb
Decreased ammoniagenesis due to hyperkalemia
Urine pH normal
There is less sodium reabsorbed which means the lumen is less negative which results in less hydrogen secreted
But the hydrogen pump is still effective so the pH is maintained
Hypoaldosteronism->less sodium in tubular lumen, change H excretion!!! Los Na with Norma function of the proton pump maintains pH of urine
Type IV RTA-related to transport system
Made worse by any drug that affects the RAAS: ACE inhibitors, ARBs, and NSAIDS
-need to know the mechanism of disruption of RAAS
Made worse by increased K intake and K sparing diuretics
-what are the K sparing diuretics
Usually a presumptive diagnosis bc it must be proven by low renin and aldosterone levels
What serum lab-24 hour urine?????? Potassium
Causes of hyposaldosterone
Hyporeninemic hypoaldosteronism: type IV RTA
Drugs CKD and DM: potentially low renin state that leads to hypoaldosteronism
K is _ with type IV
UP
Proximal RTA II
Unable reclaim filtered HCO3 in proximal tubule
When serum HCO3 is less than 15 mmol/L, proximal tubule is unable to reclaim HCO2 the urine pH<5.5
When serum HCO3 is near normal there is HCO3 spillage into urine and pH>6.5
Type 2 diagnosis
Can’t reclaim bicarb
Made by delivering HCO3 and measuring feactional excretion of HCO3
UFE HCO3>15% with bicarb
Type II
Phosphaturia, aminoaciduria, glycosuria, bicarbonaturia
Causes type II RTA
Carbonic anhydrase defiency (give for glaucoma)
Faconi
Wilson
Hyperparathyroidism, vitamin D defiency
Lead exposure
Drugs
Generalized tubular defect
Both H and K secretion are impaired
Elevated K
Urine pH>5.5
Associated with interstitial kidney disease
- SLE
- sickle cell
- obstructive uropathy
Diarrhea
HCO3 loss in stool leads to acidosis and volume depletion
K is also lost ins tool
Net effect of hypokalemia and hypobiarbemia
The hypokalemia causes increased renal production of NH4 providing urinary buffer that increases. Urine pH
How tell diarrhea from RTA??? With labs
Urine anion gap-looks at K
Chronic progressive KD
Decrease in ammoniagenesis is proportionate to the loss of nephrons
GFR<40 unable to secrete the daily acid load
Less ammonia->less anion secretion
Result: hyperchloremic acidosis
62 yo male woken up with big toe pain
Two bullet wound in army one. Removed other still in
After discharge tears out pipes and beams in old buildings
6 months headaches constipation, poor sleep, frequent urination
Big toe is swollen
Gout
Urine pH 5
Protein and glucose in urine
Gluco and proteinuria
CBC-low micro anemia, low platelets , peripheral smear see basophils stippling
PH7.29
PCO2 12
Normal anion, chronic kidney disease (BC GFR depressed)
BUN high Cr high (abnormal but proportionately so renal problem)
Uric acid high-
Waxy cast
What does he have
Lead poisoning
With agitation insomnia urinary frequency
Kidney shriveled and shrunken CKD (cortical thinning and shrinking kidney)
What expect in 24 hour urine
Ok
Harmonic tubulointerstitial disease(lead poison)
Isothenuria with polyuria
Moderate proteinuria
Very few cells
Type I, II, or IV RTA
Broad waxy casts
Small kidney
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Review
Acidosis
Metabolic or respiratory
Anion gap
Normal AG
Assess compensation
