Clinical Medicine Exam 4 Renal Flashcards
Respiratory Acidosis (general)
ineffective breathing high co2 low ph
Acute: ETOH,CNS depress, Barb, opioid OD
Status asthmaticus, mechanical hypoventilation, ARDS
Chronic: COPD, obesity, Hypoventilation, apnea, neuromuscular disorders
Respiratory alkalosis (general)
fast deep breathing, low co2 high ph
Hyperventilation, anxiety, fear, pain
If hypoxic, PE, altitude, anemia, pregnancy
Metabolic acidosis (general) (+anion gap)
low bicarb retention, low serum bicarb, low ph
MUDPILERS CAT
(CO, cyanide, aminoglycosides, toluene)
AG= NA+ (CL-HCO3)
metabolic alkalosis (general)
Rare
increase bicarb absorption, high serum bicarb, high ph
Causes = Drugs, thiazide/loop, PCN, Bicarb
S/S= Vomiting, suction/gastric, mineralocorticoid excess
Metabolic acidosis General (normal anion gap)
Diarrhea, renal tubular acidosis, Addison’s
Anion gap Calc
Na - (Cl + HCO3) = AG
Urine Anion Gap
K + NA - CL
basic idea of ammonia excretion
loss of base through GI from diarrhea causes acidosis
this causes a negative urine anion gap
Renal tubular acidosis causes a positive urine anion gap
Not useful in metabolic acidosis with anion gap due to other solutes
safest route of postassium
oral
3 steps of hyperkalemia
protect the heart
redistribute
excrete potassium
Most common cause of hypocalcemia
advanced CKD due to decreased vitamin D3
Treatment of choice for hypercalcemia with malignancy
bisphosphonates,
Thiazide diuretics and hypercalcemia
thiazide diuretics stop calcium excretion
don’t use in hypercalcemia
Most common cause of hyperphosphatemia
Advanced
Stone diagnostics
The “gold standard” diagnostic test is helical CT without contrast
Calcium Stones
UA results
Calcium Stones
higher urine calcium
higher urine oxalate
lower urine citrate
Higher urine phosphate levels and higher urine pH
Uric Acid Stone
UA results
Low urine pH
High uric acid
pH is the predominant influence on uric acid solubility
Vaccines for CKD
Covid -19 Flu TDAP Pneumo Hep B Zoster HPV MMR Varicella
SIADH
Syndrome of inappropriate antidiuretic hormone
too much ADH
Retain too much water
Hypervolemic
hyponatremic/serum osmo/hypotonic/isovolemic/urine osmo
SIADH Causes
malignancy, pulmonary disorders, CNS disorders, medications
Hyponatremia / Hypervolemia
SIADH Treatment
fluid restriction, hypertonic saline
ADH
Produced in the hypothalamus, released by the pituitary gland
Antidiuretic hormone
Most common cause of signs and symptoms of too much ADH
Low sodium
Hyponatremia
Dialysis indications
AKI (short term) ESRD stage 5 PKD (10% of pts have PKD) RCC Hypercalcemia Hyperphosphatemia Hypermagnesemia Uremia Hyponatremia (special cases)
Dialysis Risks
Hemodialysis
need access = shunt / port / fistula / graft
high risk of infection
peritoneal dialysis
risk for peritonitis
Very elderly don’t do well
Dialysis Types
Hemodialysis
3 times a week 3-5 hrs
peritoneal dialysis
(CAPD) four to six times a day manually
(CCPD) Cycles contiguously at night
ESRD Defenition
70% are due to Diabetes & HTN/CVD
ESRD Stages
Stage 5
Kidney failure
GFR less than 15
Albuminuria 4+
ESRD treatment
Dialysis
Transplant
Acute glomerulonephritis ESRD
Acute glomerulonephritis (rapid progression, ESRD in months)
CKD ESRD
Classic urine sediment finding in ESRD – waxy casts.
PKD ESRD
10% of ESRD
50% develop ESRD by age 60
Vasopressin stimulate cystogenesis which leads to ESRD
ESRD Risks
Babies born to mothers in ESRD have a mortality rate of nearly 50%
Hyperphosphatemia ESRP
Most common cause is ESRD
Ace / Arb in Nephrotic Syndrome
Tx includes Ace / Arb (also statin, loop, thiazide, GC steroids)
Ace / Arb in AKI
ACE inhibitors, ARBs causing efferent arteriole dilation
Ace / Arb in Acute glomerulonephritis
IgA nephropathy – ACE inhibitors, (maybe corticosteroids)
Ace / ARB in Renovascular HTN
If AKI occurs after initiation of ACE-I suspect RVHTN
Medical mngt – ACE-I or ARBs. BUT – both are contraindicated if bilateral stenosis present or if the patient has only 1 kidney!
Ace / ARB in Renovascular HTN
If AKI occurs after initiation of ACE-I suspect RVHTN
Medical mngt – ACE-I or ARBs. BUT – both are contraindicated if bilateral stenosis present or if the patient has only 1 kidney!
Suspect RVHTN if There is an abrupt increase of more than 25% in level of serum creatinine after admin of ACE inhibitors
Ace / ARB in CKD
HTN – ACE-I or ARBs – do this early in disease!
Proteinuria – same – ACE-I or ARBs – early
What do ACE inhibitors do?
ACEinhibitors effectively reduce systemic vascular resistance inpatientswith hypertension, heartfailureorchronic renal disease
an important part of theirlong termrenoprotective effects inpatientswith diabetic and non-diabeticrenal disease
When ACE / ARB are used together
The reduction in proteinuria appears to be greater
ACE /ARB in PKD
Single, simple cyst – observe, follow up evaluation, ACE inhibitor, ARB if HTN
HTN – 50% will be hypertensive on presentation. Cyst-induced ischemia appears to cause activation of the renin-angiotensin system. Use an ACE inhibitor or an ARB
ACE /ARB in Hyperkalemia
Causes – ACE inhibitors, angiotensin-receptor blockers,
(potassium-sparing diuretics, or the combination, mineralocorticoid deficiency or CKD, genetic disorders, urinary tract obstruction)
ACE inhibitors, ARBs and spironolactone, potassium-sparing diuretics should be used cautiously in patients with heart and/or liver failure and kidney disease
ACE /ARB in Metabolic alkalosis
If saline unresponsive – may need surgical removal of mineralocorticoid producing tumor – if not – ACE inhibitor or Spironolactone
AHA BP Goal
130/80
GFR
Useful measure of kidney function at the level of the glomerulus
Measured directly via biomarkers (most commonly creatine)
Measures the amount of plasma ultrafiltered across the glomerular capillaries
Reflects the ability of the kidneys to filter fluids and various substances, including medications.
(eGFR) Estimation of Glomerular filtration rate
GFR
volume of plasma filtered per unit time
Useful measure of kidney function at the level of the glomerulus
Measured directly via biomarkers (most commonly creatine)
Measures the amount of plasma ultrafiltered across the glomerular capillaries
Reflects the ability of the kidneys to filter fluids and various substances, including medications.
GFR controlled by adjusting glomerular blood pressure from moment to moment
Traditionally calculated by the creatinine clearance (requires 24 hour urine collection)
Normal values vary significantly
(eGFR) Estimation of Glomerular filtration rate
MAP and GFR
Changes in MAP could impact GFR by changing Glomeular Capillary Pressure (PGC)
GFR stability
Between 80 – 180 mmHg, GFR does not change much with changes in MAP because of
intrinsic regulatory mechanisms
GFR Averages
Average GFR = 125 ml/min
180 L filtered daily
Only 1.5 L urine made daily
Most filtered fluid is reabsorbed
Criteria for AKI
RIFLE
Criteria for AKI
RIFLE
Risk, Injury, Failure, Loss, End-stage
Most at risk for Wilms tumor
Most common in children under 5 years old
Most common cause of abdominal mass in children
Represents 5-6% of cancers in children younger than 15 years
Wilms tumor Tx
TX – total nephrectomy plus chemotherapy
Up to 90% cure rate.
Clinical signs of Wilms tumor
palpable abdominal mass does NOT cross midline,
hematuria, nausea, vomiting, HTN, anorexia – may be present.
Mass may be only clinically apparent finding
CBC usually normal, may have anemia
increasing size of abdomen or an asymptomatic abdominal mass. About 25% are hypertensive on presentation. Microscopic hematuria in approximately 25% of patients, gross hematuria is rare
Renal Cell Carcinoma Clinical presentation
Tumor of the proximal convoluted renal tubule cells
highly metabolic
Renal Cell tumors are by far the most common tumor originating in the kidney (~95%)
Difficult to diagnose due to typically being asymptomatic.
Once diagnosed – difficult to treat – resistant to chemo and radiation
Most common is clear cell RCC
RCC Risk Factors
smoking, obesity, dialysis, obesity, being a male (2-1), HTN, rare genetics
Nephritic Syndrome
Post infectious: MCC = Strep throat, skin infections
Wegner’s granulomatosis, polyarteritis nodosa
Goodpasture’s syndrome, neuropathy, purpura
Nephritic is always associated with hypertension
proteinuria less than 3.5 g/day
Tx = Steroids
Nephritic Syndrome
Post infectious: MCC = Strep throat, skin infections
Wegner’s granulomatosis, polyarteritis nodosa
Goodpasture’s syndrome, neuropathy, purpura
Nephritic is always associated with hypertension
proteinuria less than 3.5 g/day
Tx = Steroids
Nephrotic Syndrome
Proteinuria > 3.5g/DAY
Most common in children
Focal segment glomerulosclerosis” – HIV, heroin, HTN
African American patients
Hypoalbunemia
Hypercholesterolemia
edema
Doesn’t cause hypertension
Tx
glucocorticoids (SLE or MCD), loop or thiazide diuretics, ACE or ARB, statin
Nephritic syndrome and glomerulonephritis
Less extra, more benign, when severe it is termed rapidly progressive glomerulonephritis
Nephritic syndromeandacute glomerulonephritis.Glomerulonephritisrefers to a number of kidney problems that involve inflammation in the glomeruli, which are the kidney’s filtration units.Acute glomerulonephritiscan causenephritic syndrome.
AKI intrinsic
Acute Glomerulonephritis
Intrinsic Kidney Injury (AKI)
Several etiologies – post-infection (think strep)
Tx: All forms except the rapidly progressive forms are typically self-limiting
(rapid or progressing disease = steroids/cyclophosphamide)
Edema, HTN, hypervolemia – Loop diuretics, beta-blockers, CCBs
Post strep AGN- maybe antibiotics (PEN G)
Protein + hematuria with acanthocytes + red blood cells casts – highly suggestive of glomerulonephritis
(RBC Casts)
Hydronephrosis
Not a disease
ALWAYS caused by obstruction (renal calculi, BPH, neoplasm)
quite rare
UA usually neg, might have increase creatinine
Ultrasound
– usually asymptomatic – may notice change in urinary output, may be hypertensive
TX – remove obstruction
Meds – adults with hydronephrosis, complicated by infection – should be treated with abx for 3-4 weeks
Hydronephrosis with infection is a urologic emergency – treated by prompt drainage using retrograde stent insertion or percutaneous nephrostomy
AKI intrinsic
Acute tubular necrosis
Most common type of AKI
Acute destruction and necrosis of the renal tubules of the nephron
endogenous nephrotoxins or prolonged prerenal azotemia
If due to prerenal azotemia – often present hypotensive and/or hypovolemic
Exogenous toxic Causes:
dye, Vanco, aminoglycosides, NSAIDS
Endogenous causes:
Tumors, cancer, Rhabdo
Urinalysis - ”Muddy Brown Casts”,
TX – first – IV fluids and remove offending agent(s)
UA = BUN 10-15:1
Urine osmo: 300
Urine Na: >40
FENA >2%
AKI Pre renal
poor perfusion
BUN: creatinine ratio > 20:1
TX – replace volume
When is BUN: Creatinine ratio reliable?
When not pulled from a heparin line
AKI Post renal
Rare
Always obstructive
Causes BPH, BOO, Tumors, stones/strictures
BUN Creatinine ratio 10:1
usually asymptomatic
Ultrasound
TX remove obstruction
AKI Intrinsic
Acute interstitial nephritis
Acute tubular necrosis
Acute glomerulonephritis
Normal BUN creatinine ration 10-15:1
AKI Intrinsic
Acute interstitial nephritis
inflammatory response in the interstitium
most common cause is drug hypersensitivity (70%)
drug causes: SCCRAP
also infection, auto immune, unknown
Fever, arthralgia, rash, eosinophils
Tx remove offending agent
(usually a spontaneous recovery)
normal kidney function back in one year
PKD
Adult onset
autosomal dominant disorder
Most common hereditary kidney disease
Autosomal recessive in infants
multi system
Abdominal pain, flank pain, nocturia, berry aneurysm, mitral valve prolapse
large palpable kidneys, HTN, protein/blood in urine
Ultrasound, genetic testing
simple single cyst - follow up ACE/ARB if HTN
Fluids, control HTN, treat UTI’s (preserve renal function
ESRD = dialysis / transplant
10% of ESRD
50% develop ESRD by age 60
Vasopressin stimulate cystogenesis which leads to ESRD
Renal vascular disease
Renal vascular hypertension
Large vessel atherosclerosis, muscular diseases, embolotic disorders, inflammation,
blood supply changes are followed by fibrosis and loss of kidney function
Horseshoe kidney
1 in 1000 have some sort of fusion
(most common is horseshoe kidney)
always contains 2 ureters
may have alternate blood supply
Kidney biopsy
AGN and CKD
Nephritic syndrome
Biopsy should be considered in AKI patients with no apparent cause
Possible osteodystrophy (brown hemosiderin (cystic brown tumor)
Kidney Imaging
Renal osteodystrophy = x ray
Kidney Imaging
Renal osteodystrophy = x ray
Hydronephrosis = UA
(antegrade urography can be used also in AKI)
Stones = CT wo contrast, US preferred initially
small kidneys are seen with US
Which of the following is not a cause of Hyperkalemia?
A. Rhabdomyolysis
B. K+ sparing Diuretics
C. Metabolic Alkalosis
D. Metabolic Acidosis
C. Metabolic Alkalosis
Rhabdo causes cell lysis
K+ is out
Both cause solute shift but Meta alk causes hypokalemia
Of the following, which are body systems that manifest clinical signs and symptoms of hyperkalemia?
A. Neuro/muscular and Cardia
B. Cardiac and GI
C. MSK and GI
D. Neuro/muscular and GI
A: neuro muscular cardiac
Protect the heart
causes impaired neuromuscular junction
What is the earliest sign of hyperkalemia on an ECG?
A. Prolonged PR interval
B. Peaked T waves
C. Widening of QRS
D. QT shortening
Peak T waves is early sign of hyperkalemia
QT shortening is hypercalcemia
Wide QRS is late hyperkalemia
Severe Hyperkalemia is Prolonged PR
