Genitourinary Exam 1 Cards Flashcards
9 major renal functions
Excretion
Water and Electrolyte balance
Fluid volume
Plasma osmolality
RBC production regulation
BP regulation
Acid base balance
Vitamin D activation
Gluconeogenesis
How does the kidney regulate RBC production?
It releases erythropoietin in response to hypoxia
How does the kidney modulate blood pressure
Releases renin in response to low flow
Renal medulla and cortex on biopsy
Cortex = Spaghetti and meatballs
Medulla = Bundles of pencils
Scar tissue
Not metabolically active and therefore does not need as much oxygen
More common nephron type
Cortical
Podocytes
Surround capillary loops in the glomerulus to remove trapped material and contract capillaries if needed
Most common complaint and complication associated with a horseshoe kidney
UTI - Bacteria grow in pooling urine
Ureteropelvic junction obstruction
Kidney stones
Diagnosis and treatment of a horseshoe kidney
CT, Urinalysis, and Renal function
Manage disorders and complications as they arise
Urine filtrate
Plasma without proteins
Glomerular Filtration rate
Amount of filtrate formed over time
Resorption of PCT
60% of HCl and H20 90% of bicarb
Secretes most wastes (urea, ammonia, creatinine, etc.)
Loop of henle
Water goes out the descending
Sodium goes out the ascending
Most magnesium resorbed
Where do loop diuretics work
Thick ascending loop of henle
Distal Convoluted tubule
May resorb urea
CALCIUM regulation Secretes K+
Regulates pH
Site of action for thiazide diuretics
Cortical collecting duct
Resorbs NaCl and H2O
Secretes K+
Aldosterone and K sparing diuretics work here
Medullary collecting duct
Final modification of urine with some secretion and resorption
How do nephrons handle loss
They do not regenerate but hypertrophy in order to compensate for lost tissue
Maladaptive deterioration
Point at which nephrons can no longer compensate for losses
Amount of renal mass removal resulting in ESRD
80%
Progression of nephron loss
Damage to glomeruli (via HTN) results in protein leakage which leads to inflammation and fibroblast activation
GFR of CKD
Under 60mL/min
2 Limitations of GFR
Can’t detect problems that are non-glomerular
May go up at the onset of renal disease
May appear stable in worsening disease
3 substances that can be used for GFR estimation
BUN, Creatinine, Cystatin C
Factors effecting GFR estimation
Body surface area - smaller body=less muscle mass
Age - declines with age
Gender - Males have more muscle and more creatinine
Race - AAs have more muscle and more creatinine - new recomendations don’t use race
3 factors that increase serum creatinine that are NOT renal failure
Meat intake
Creatine supplements
High muscle mass
Medications that inhibit renal secretion of creatinine
Abx - cephalosporins, aminoglycosides, trimethoprim
Cimetidine
Effect of liver disease on estimated GFR
Decreases creatine production leading to decreased creatinine, leading to higher eGFR
Creatinine clearance in CKD
Enhanced in early stages, taken over by liver in late stages
Creatinine Clearance
Requires 24 hour collection of urine for creatinine testing and estimates the upper limit of the true GFR
When does one need to finish collecting urine for a CrCl test
within 10 minutes of the 24 hour mark of beginning
Limitation of CrCl urine test
Cumbersome and has a tendency to overestimate
Cause of BUN:Cr above 20:1
Dehydration due to increased renal resorption - tubules must be working
Cell breakdown can also cause incresed BUN as well as decreased renal perfusion
4 things causing decreased BUN
Liver disease
Malnutrition
Sickle cell anemia
SIADH
BUN and GFR estimation
Less useful for estimation - much of it is resorbed is inversely proportional to GFR, and can change independantly
Cyastatin C and GFR
Not as impacted by race, gender, age as creatinine but still increased by things like male sex, fat mass, diabetes, etc.
Inverse relationship and EXPENSIVE
3 indications for cyastatin C measurement
Elderly patients
Body builders
Acute Illness
(All have abnormal muscle mass)
Cockroft Gault equation
Estimates CrCl in a patient with stable Cr
Need age and body weight, sex
Overestimate
MDRD study equation
Estimates GFR with body surface area and Cr
Needs age, sex, race
More accurate than CG
CKD-EPI Study
More accurate GFR measurement than CG works best for mild or normal GFR
Better risk prediction
Uses serum creatinine, age, and sex (no longer modified by race)
Preferred GFR equation in US
CKD-EPI (no race)
Acute kidney injury
Sudden decrease in kidney function over hours or days with inability to manage fluid electrolytes, and acid base or excretion of waste products
Duration of AKI before we see a drop in labs
Can be up to 12-24 hours
Azotemia
Increase of waste products in the blood
Uremia
Symptomatic azotemia
Anuria
Under 50 mL in 24 hours
Oliguria
50-400 mL in 24 hours
Polyuria
2500-3000 mL/day or more
6 uremic symptoms
Weakness, tremors, dryness, HTN, Nausea, acidosis
Most common cause of AKI
Prerenal azotemia (followed by intrinsic)
Prerenal azotemia
Azotemia due to inadequate renal perfusion, hypovolemia, decreased cardiac output, or changed vascular resistance
BUN/Cr ratio of prerenal azotemia
Greater than 20:1 because kidneys think we are dehydrated
Fractional excretion of sodium in prerenal azotemia
Under 1% - kidneys think we are dehydrated - retain sodium
Clinical presentation or prerenal azotemia
Dehydration, Sepsis, diffuse abdominal pain and ileus
MCC of postrenal obstruction in men
BPH
2 tests for postrenal obstruction
Bladder catheterization and/or abdominopelvic US
BUN/Cr ratio of postrenal obstruction
Over 20:1
Urine osmolality of postrenal obstruction
400mosm/kg or less
3 major causes of Acute Tubular Necrosis
Ischemia
Nephrotoxins
Sepsis - hypoperfusion or direct injury
5 Nephrotoxic antimicrobials
Gentamycin, Streptomycin (less so), Vancomycin, Sulfonamides, Cephalosporins
2 nephrotoxic antivirals and one antifungal
acyclovir, foscarnet, amphotericin B
3 non pharm exogenous nephrotoxins
Radiographic contrast media, Chemo/immunosuppressants, Heavy metals etc.
Myoglobinuria
Due to rhabdomyolysis - urine appears dark brown but no detection of RBCs. False positive for hemoglobin
Treatment for myoglobinuria
Rehydrate - may have high electrolytes and low calcium which correct
3 other endogenous nephrotoxins
Hemoglobinuria (hemolysis)
Hyperuricemia (chemo - uric acid over 15-20 mg/dL)
Bence Jones protein - Obstructs tubules, multiple myeloma
Clinical presentation of acute tubular necrosis
Uremia and arrhythmias may be noted
Low GFR with BUN:Cr under 20:1
Muddy brown casts
Elevated urine sodium
What does low BUN:Cr or elevated urine sodium mean
We are NOT resorbing anything
Treatment for Acute tubular necrosis
Avoid volume overload, loop diuretics, or dialysis
Promote dietary interventions
Better long term outcome ATN patient
Non-oligouric
Classic presentation of acute glomerulonephritis
HTN, Edema, urine containing protein, RBCs, WBCs, and RBC casts
Crescent lesions
Severe breaks in glomerular walls
Types of Glomerulonephritis
Immune complex destruction
Anti-GBM autoantibody destruction
C3 deposition
Pauci-immune (vasculitis)
2 places edema is seen first
Scrotal and periorbital
Treatment for acute glomerulonephritis
Corticosteroids - high dose
Plasma exchange for goodpasture or pauci immune
Immune complex glomerulonephritis
Antigen-antibody complex lodges in GBM leading to its destruction by the immune system
Anti-GBM associated glomerulonephritis
Autoantibodies against the GBM are produces - called Goodpature syndrome if the lungs are also effected
C3 glomerulopathy
Caused by C3 deposition in the glomerulus - may result in low C3 levels. Minimal role played by immune globulins
Monoclonal Ig-mediated glomerulonephritis
Monoclonal antibodies lodge in the GBM - no antigens are seen
Can be detected with serum protein electrophoresis
Pauci-Immune GN
Associated with ANCAs (anti-neutrophillic cytoplasmic antibodies)
No immune complexes or complement involved
MCC of acute interstitial glomerulonephritis
Medications
Can also be infectious or immune
Classic triad of interstitial glomerulonephritis
Fever, rash, arthralgia (may not see ALL three)
Urine sediment of AIN
WBCs, RBCs, No protein
BUN:Cr ratio of Acute interstitial GN
under 20:1
BUN:Cr ratio for Glomerulonephritis
Greater than 20:1
Broad or waxy urine casts
Chronic renal failure
Hyaline casts
Exercise, diuretics, concentrated urine
Fatty casts
Nephrotic syndrome (oval fat bodies)
Granular casts
Chronic renal failure or ATN
Renal tubular epithelial cast
ATN
RBC casts
Glomerulonephritis
WBC casts
Interstitial or pyelonephritis
2 diagnostics to rule out urethral obstruction
Urethral cath and bladder scan US
4 things that increase and one thing that decreases when total body water drops
Increase:
SNS
RAAS
ADH
Thirst
Decrease:
ANP
Clinical presentation of isotonic fluid volume defecit
Altered mental status, low BP high HR, Weak pulse, Dry mucous membranes
Why does professor Jensen love lactated ringers?
They don’t have sodium in them
Treatment for volume overload
IV diuretics (loop), dialysis if no response to therapy, Restrict fluids and sodium
Clinical presentation of hyperphosphatemia
SOB, N/V, Hypocalcemia (hyperreflexia, trousseu and chvostek signs, carpopedal spasm
Clinical presentation of hypokalemia
Weakness, constipation, flattened T waves and ST depression
Clinical presentation of hyperkalemia
Cramps, diarrhea, vomiting, hypotension, palpitations
Peaked T waves, lost P waves, Wide QRS
Treatment for hyperkalemia
Treat if EKG changes or neuromuscular symptoms
Block cardiac effects
Reduce plasma K+
Remove potassium
Blocking of cardiac effects in the hyperkalemic patient
IV calcium gluconate with cardiac monitoring
Repeat if EKG changes do not occur
Can potentiate toxicity of digoxin
Reducing plasma potassium in hyperkalemic patient
Administer insulin followed by dextrose
Albuterol can also help
Removal of potassium in the hyperkalemic patient
GI cation exchangers (Kayexalate, zirconium cyclosilicate, patiromir)
Loop or thiazide diuretics
Dialysis - can even electrolytes
Isotonic hyponatremia
Usually means that there are extra molecules in the blood (fat or protein), skewing the data
Correct underlying cause
Hypertonic hyponatremia
Another osmotically active molecule is present such as glucose or radiocontrast
Correct underlying cause
Hypovolemic hyponatremia
Due to inappropriate salt loss (ie. GI, burns, dehydration)
Renally due to ACEIs, Diuretics, aldosterone deficiency, renal salt wasting
Hypovolemic hyponatremia
Sodium is retained but even more water is retained - nephrotic syndrome, intrinsic renal fluid retention, heart failure, liver disease
Euvolemic hyponatremia
SIADH, hypothyroidism, psychogenic polydipsia, beer potomania
Clinical presentation of hyponatremia
Primarily neurologic due to cerebral edema
Confusion, lethargy, seizure
Less symptoms when chronic
Treatment of hypovolemic hyponatremia
Rehydration with normal saline
Use hypertonic saline if the condition is severe
Treatment difference in chronic and acute hypernatremia
Acute - correct in 24 hours
Chronic correct more gradually
pH at which bicarbonate treatment is generally needed
pH under 7.2
Treatment for chronic metabolic acidosis in CKD
Bicarb replacement
Decreasing animal products in diet
Mechanism of metabolic acidosis in AKI
Kidney unable to excrete acid and regenerate Bicarb
How does acidosis affect potassium balance
It leads to hyperkalemia
Situations in which to administer bicarb in severe AKI acidosis
Due to diarrhea
Waiting for dialysis
AKI readily reversible
Rhabdomyolosis without other dialysis indications
Situations in which to dialyse in AKI acidosis
Severe AKI with volume overload
If organic acidosis from lactic or keto acids
pH under 7.1
Risk of volume overload if giving sodium
Indications for dialysis in AKI
Azotemia and Uremia
Life threatening electolyte disturbances
Volume overload unresponsive to diuretics
Acidosis below 7.1
Official definition of CKD
Presence of markers of kidney damage or GFR under 60 for 3+ months
Kidney nephron response to a decrease in the number of functional nephrons
Hyperfiltration and Hypertrophy
Cardiorenal syndrome nameing
Acute or Chronic is for BOTH organs
Renocardiac is the kidneys fault, Cardiorenal the hearts fault
GFR CKD stages
1-5 w/ 3a and 3b
1 is normal (90+)
2 - 60-90
Down by 15 after than
Albuminuria stages
A1 - Under 30 mg/g
A2 - 30/300
A3 - 300+
Isosthenuria
Urine is the same concentration as blood
Uremic frost
Crystallized urea excreted in sweat
Cause of broad waxy casts in CKD
Dilated (Hypertrophied) Nephrons
Clinical presentation of CKD in stages 1-2
Edema and HTN most common or signs of underlying disease
Clinical presentation of stages 3 and 4 of CKD
Anemia, fatigue, anorexia, Abnormal calcium, phosphorous, vitamin D, PTH, Sodium, potassium, and water
Clinical presentation of stage 5 CKD and ESRD
Marked disruption of ADLs and well being
Medication most used for CKD
ACE/ARB - BUT don’t use in AKI!!
CVD in CKD patients
Usually death is from cardiac complications before kidney problems
CKD patients build plaques faster and at lower cholesterol levels
Goal BP for CKD patients
Less than 130/80mmHg okay if a little over
ACEI/ARBs in CKD - monitoring
Check creatinine and K+ 7-14 days after starting or increase and reduce or stop drug if it has gone up over 30%
Diuretics in CKD
Thiazides early on
Loop more effective when GFR is under 30
Over diuresis can cause AKI
Drugs for lipid management in CKD
Statins = First line and recc’d for most pts
PSK-9 inhibitors and ezetimibe as adjunct therapy
Fibrates as last resort (can cause rhabdomyolosis
Electrolyte abnormality to monitor for in ACE/ARB use
Hyperkalemia
Atrial fibrilation treatment risk in Stage 5 and ESRD patients
Greater bleeding risk with anticoagulation
Pericarditis in CKD
Retrosternal chest pain with friction rub, low voltage QRS, ALWAYS an indication for dialysis
Typical mineral metabolism abnormality in CKD patients
Hyperphosphatemia
Hypovitaminosis D
Hypocalcemia
Osteitis fibrosis cystica
MC form of renal osteodystrophy
Hyperphosphatemia leads to hyperparathyroidism which leads to osteoclast stimulation
High rates of bone turnover
Adynamic bone disease
Suppression of PTH or low endogenous PTH = LOW bone turnover
X-ray finding of osteitis fibrosa cystica
Brown tumors (hollow looking spots) on bones
Controlling hyperphosphatemia in CKD mineral metabolism abnormalities
Initially use dietary intervention, later use oral phosphate binders
CKD phosphate binders
Calcium carbonate (Tums, watch for atherosclerosis or hypercalcemia)
Sevelamer or Lanthanum (Non-calcium first line)
Aluminum hydroxide
Management of PTH levels in CKD mineral metabolism abnormalities
Vitamin D3 (calcitriol) use to balance vitamin D
Cinacelcet - Increase sensitivity of the parathyroid gland good if increased phosphorus or Ca exclude calcitriol
Hepcidin
Blocks GI iron absorption
Treatment for iron deficiency in CKD
Ferrous sulfate, gluconate, fumarate, or citrate are approved
No iron if ferritin is over 500-800 ng/mL
Erythropoietin treatment in CKD
Hold EPO until Hgb drops below 10
Goal is 10-11 for Hb numbers
Epo dosing regimens and side effect
Epoiein 1-2x per week
Darbepoietin every 2-4 weeks
HTN seen in 20% of patients
Treatment for hematologic coagulopathy
Due to PLT dysfunction
Only treat if symptomatic
Desmopressin and dialysis can help
Cryoprecipitate is rarely used
Severe protein loss can lead to HYPERcoagulability
Good diuretics for high potassium
Loop diuretics
Cause and treatment for metabolic acidosis of AKI
Loss of ability to excrete acid, maintain serum bicarb at 21+mEq/L
Uremic encephalopathy
Due to aggregation of uremic toxins
Difficulty concentrating to altered mental status
Uremic neuropathy
Indication to start dialysis
Symmetrical mixed neuropathy
Loss of vibration to clonus/muscle atrophy
Paresthesias
Hypoglycemia of CKD
Due to decreased renal clearance of insulin
d/c metformin when Cr is above 1.4 or GFR is under 30
CKD pregnancy
50% infant mortality rate
surviving infants are often premature
CKD progresses faster
Sodium restriction for CKD
2g/d
CKD protein restriction
May slow progression - careful if cachectic
Water restriction for CKD
2L/d
Potassium restriction for CKD
Less than 2g/d (50-60mEq) if GFR under 10-20 mL/min or hyperkalemic
Medications to avoid or manage in CKD
Renally excreted drugs
Mg or Ph containing drugs
Morphine
NSAIDs and IV contrast (nephrotoxic)
Indications for dialysis in CKD
When GFR reaches 5-10 mL/min
Uremic symptoms
Refractory metabolic disturbances
Unresponsive fluid overload
Risk of peritoneal dialysis
Removes large amounts of albumin
Patients with abdominal surgeries may not by good candidates
Diagnostic conditions for peritonitis
Over 100 WBC/mcL in peritoneal fluid with over 50% PMN
MCC staph
Nephritic spectrum
Has more to do with inflammation
Under 3g/d proteinuria
Hematuria with RBC casts
Nephrotic spectrum
Has more to do with proteinuria
Over 3g/day proteinuria
Bland urine sediment with oval fat bodies potentially
Bergers disease
IgA nephropathy
Coca cola colored urine
Form of nephritis
Clinical presentation of nephrotic syndrome
Hypoalbuminemia causing edema
Hyperlipidemia
Immune complex deposition glomerulonephritis
Antigen-antibody complexes lodge in the GBM. GBM is destroyed in immune crossfire
Often associated with Strep infections, Berger disease, Lupus
Anti-GBM associated glomerulonephritis
Autoantibody formation against the GBM
Called Goodpasture’s syndrome when it involves that Lungs AND Kidneys
C3 glomerulopathy
C3 complement proteins lodge in the GBM causing its destruction -caused by an abnormal alternative complement pathway
Monoclonal Ig-mediated glomerulonephritis
Excessive antibodies lodge in the GBM due to multiple myeloma or MGUS (monoclonal gammopathy of Undetermined significance)
Pauci immune glomerulonephritis
Small vessel vasculitis associated with antineutrophilic cytoplasmic antibodies (ANCAs) caused by cell mediated autoimmune processes
Clinical presentation of nephritis
Cola colored urine
Edema (periorbital and scrotal first) and HTN
Uremia eventually
Glomerulonephritis associated with ANCA levels
Pauchi immune GN
Purpose of an ASO titer
Helps evaluate for a recent streptococcal infection
2 types of glomerulonephritis for which plasma exchange is recommended
Goodpasture disease
Pauci-immune GN
General treatment for glomerulonephritis
Manage HTN and volume
May use high dose corticosteroids for immunosuppression
Post infection glomerulonephritis
Bacterial or viral
MCC is GABHS
1-3 weeks after infection
Treatment for post infectious glomerulonephritis
Support - antihypertensives, salt restrict, diuretics
Steroids are NOT helpful
Henoch Schonlein purpura
Systemic small vessell vasculitis associated with IgA deposition in vessel walls
Purpura in lower extremities -supportive care
MCC and criteria for nephrotic disease
DM is MCC
Over 3g of proteinuria/day
Subnephrotic proteinuria
Proteinuria with few s/s
Nephrotic syndrome
Peripheral edema seen with proteinuria
Places we first see edema in nephrotic syndrome
Around eyes and scrotum
Gross hematuria
We don’t need a microscope to visualize the blood
Urine sediment of nephrotic syndrome
Oval fat bodies
Grape clusters
Maltese crosses with polarization
Hypoalbuminemia
Serum protein under 3g/dL
Hypoproteinemia
Serum protein under 6g/dL
Why is ESR elevated in nephrotic syndrome?
Loss of proteins C and S
When might we do a renal biopsy
When there is not an obvious cause such as DM
Treatment for proteinuria in nephrotic syndrome
Increase dietary protein if loosing 10+ g/d
ACE/ARB to lower urine protein excretion by reducing glomerular capillary pressure
Treatment for edema in nephrotic syndrome
Dietary salt restriction
Need larger doses of thiazide/loop diuretics bc they are protein bound
Minimal change disease
A primary nephrotic syndrome
Common in children
Treat with prednisone for 8 weeks (children) or 16 weeks (adults
Membranous nephropathy
Common in adults - immune complex deposition OR secondary to NSAIDs, cancer, etc.
May be asymptomatic or frothy urine
Treatment for membranous nephropathy
ACE/ARB, Immunosuppressive agents, Transplant
50% progress to ESRD, 30% spontaneous remission
Kidney v. bladder bleeding
Kidney will be more brown
Bladder will be more red
(just like GI tract)
One size fits all response of the kidneys
Increase the RAAS
Most common presenting symptom in Berger disease
episode of gross hematuria
One thing that must be done when an acute on chronic kidney injury occurs
Stop ACE/ARB
Amyloidosis
Secondary nephrotic syndrome due to extracellular deposition of amyloid protein
Low GFR, Enlarged kidneys
Limited treatment
Progress of diabetic nephropathy
Hyperfiltration
Microalbuminuria (30-300 mg/dL)
Albuminuria
When to treat diabetic nephropathy
As soon as microalbuminuria is found
Glycemic control
HTN treat to goal
ACE/ARB
MCC of acute interstitial nephritis
Medication
3 causes of chronic Tubulointerstitial Disease
Obstructive uropathy
Vesicoureteral reflux
Anagesic nephropathy
How much analgesic tends to lead to nephropathy
1g/d for 3+ years
Causes of obstructive uropathy
Enlarged prostate
Stones
cancer
Retroperitoneal fibrosis
Leads to reflux and scarring
Potential s/s of obstructive uropathy
Pain - with a stone
Bladder distension
HTN
Can all be normal!!
Labs for obstructive uropathy
May present with polyuria due to damaged tubules
Benign UA may have pyuria/hematuria
Elevted serum creatinine
Imaging for obstructive uropathy
Should be done on all AKI and CKD patients with unknown cause
US is preferred, CT for stones
Vesicoureteral reflux
Retrograde flow of urine while voiding due to misplaced sphincter
Clinical presentation of vesicoureteral reflux
Frequent UTIs esp. in young children
HTN
May have mild/moderate proteinuria
Imaging findings for vesicoureteral reflux
Assymetric kidneys - one will usually compensate for the other
Can use a US, CT, or Voiding cystourethrogram
Treatment for vesicoureteral reflux
Maintain sterile urine in childhood
Surgical reimplantation (only works in children
ACE/ARB for HTN
Analgesic nephropathy
Tubulointerstitial and papillary necrosis
Analgesics can be VERY concentrated in papillae
Urine and imaging findings of analgesic nephropathy
Sloughed papillae in the urine
Small scarred kidney with calcifications on CT
Ring sign or golfball on tea seet with CT contrast
Treatment for analgesic nephropathy
Renal decline stabilizes or improves slightly with analgesic removal
Clinical findings of autoimmune interstitial nephritis
Polyuria w/ dilute urine, Volume depletion, Acidosis
Kidney scarring
Treatm underlying issue
Nephrocalcinosis
Deposition of calcium in the renal parenchyma and tubules
Cauliflower florets in the kidneys
Cause and risk factors for nephrocalcinosis
Increased urinary excretion of calcium, phosphate, or oxalate
Hyperparathyroidism
Vitamin D
Loop diuretics
Clinical presentation of nephrocalcinosis
Often asymptomatic
May have hypercalcemia or hyperphosphatemia
Minimal proteinuria
Imaging for nephrocalcinosis
US is best can use CT
Single renal cyst
Usually not concerning and found incidentally
No HTN or ESRD signs present
Routine management of benign renal cyst
Routine follow up
More likely to be cancerous if they have developed after initiation of dialysis
Childhood medullary kidney disease
Juvenile Nephronophthisis
Autosomal recessive
Renal cysts in the corticomedullary junction and in the medulla
Adult medullary kidney disease
MCKD - 20-70yrs
Autosomal dominant
Renal cysts in the corticomedullary junction and in the medulla
S/S of medullary kidney disease
Hyperuricemia
HTN
Growth restriction for juvenile
Treatment for medullary cystic kidney disease
No therapy to stop progression
Allopurinol for hyperuricemia
Does not recur in renal transplants
s/s of Autosomal dominant PKD
Abdominal or flank pain
UTI/Stones
Palpable kidneys
Hematuria
Ultrasound to confirm
Can get cerebral aneurysms in the COW
Two other places to check for cysts in PKD
Spleen and liver
Tx for pain and hematuria associated with PKD
Analgesics, decomprassion for pain from bleeding, infection, stones
Hydration for bleeding, recurrent may be carcinoma
Cerebral aneurysms PKD screening
Usually not recommended
Antibiotics with cystic penetration for PKD
Quinolones, Bactrim
Medications for ADPKD
Vasopressin receptor antagonists:
Ocreotide - decreased cyst growth
Tolvaptan
4 risk markers indicating use of Tolvaptan in ADPKD
Mayo class 1C-E
Under 55 w/ GFR under 65
Kidney length over 16.5 cm in 50y/o
PROPKD score 6+
Patients 18+ with GFR 25+ and one of the above should be on something
3 things that may slow progression of ADPKD
Avoidance of caffeine
Protein restriction
HTN Tx
BBW for tolvaptan
Should be initiated in a hospital where serum sodium can be closely monitored
CI in liver disease, may cause thirst/polyuria
Location of cysts in ARPKD
Cysts on collecting tubules only
Metabolic acidosis and HTN
Oligohydramnios (low amniotic fluid in utero)
Presentation and treatment of autosomal recessive PKD
Cysts only visible after birth - no disease in parents
Manage HTN
Dialysis and transplant
2 causes of renal artery stenosis
Atherosclerotic disease (by far most common)
Fibromuscular dysplasia (suspect in women under 40 w/ unexplained HTN)
s/s, PE and labs for renal artery stenosis
Refractory or new onset HTN
AKI after ACEI
Abdominal bruit
Elevated BUN/Cr with ischemia
Imaging for renal artery stenosis
Doppler US can show small or asymmetric kidneys on regular US
CT angiography may be less accurate and more expensive
MRA excellent but expensive
Renal angiography = Gold standard
Treatment for renal artery stenosis
Medical management of HTN
Stenting produces good results
Bypass not superior
Nephrosclerosis
Hypertensive nephropathy with sclerosis and interstitial fibrosis
More common in African Americans
Give ACE/ARB or thiazide diuretic
Cholesterol atheroembolic disease
Emboli to the kidneys from vascular plaques, angiography is a risk factor
s/s of cholesterol atheroembolic disease
1-2 weeks after inciting event
Worsening of HTN and renal function
May see livedo reticularis or localized gangrene
Livedo reticularis
Webbing patter on legs
Labs for cholesterol atheroembolic disease
Increased eosinophils, Cr, ESR
Def dx - kidney biopsy
Statins are most recommended
MC kidney cancer
Renal cell carcinoma
Risk factors for renal cell carcinoma
May be familial or dialysis related
HTN, analgesics, Obesity
SMOKING - biggest
Clear cell carcinoma
Most common type of kidney cancer
Papillary tumors are less common but happen
Clinical presentation of renal call carcinoma
Hematuria = most common
May see flank pain or abdominal mass
Cough or bone pain in metastasis
Usually found incidentally
Stauffer syndrome
Abnormal liver function enzymes w/o metastasis - may just be a result of the carcinoma
Imaging for renal cancer
US - for initial
CT to look at mass
MRI, Bone, Brain for mets
Initial labs for renal cancer
CBC, LFT, UA
Difference of PKD and cancer
PKD is more definied and evenly spread out
Treatment for RCC
Radical nephrectomy
Chemotherapy has limited efficacy
Wilms Tumor
Seen in pediatric patients
Due to abnormal kidney development - single unilateral lesion
Clinical presentation of Wilms tumor
Abdominal pain
HTN
Hematuria
Imaging for wilms tumor
US for first
CT/MRI for follow up
CBC,CMP, UA, Coag (you’re gonna do surgery)
Wilms tumor treatment
Surgical resection - prognosis is often good
Recurrent disease is possible
Oncocytoma
Common benign tumor that looks like RCC - treat like RCC
Angiomyolipoma
Fat muscle and vessel tumor MC in women
Benign but can bleed
Embolize
Organs that metastasize to kidney
Lung, stomach, other kidney
Risk factors for kidney stones
Dehydration
High protein/salt intake
Gout
Most common type of kidney stones
Calcium oxalate or phospjate
Visible on X-ray
Clinical presentation of kidney stones
Acute severe flank pain - may follow ureters and be episodic
Nausea and vomiting
Urinary stone labs
Hematuria
May have an abnormal pH of urine (high for calcium, low for uric acid)
Litholink
Panel specifically looking for stones
Imaging for renal stones
X-ray
US for pregnancy
CT - shows ALL stones
Staghorn calculus
Stone that grows up into calyces
Treatment for kidney stones
Try NSAIDs if not tried
IV fluids don’t help
Opioids may be needed for pain
Tamsulosin (a blocker)
Steroids
Obstruction with infection
Medical emergency
CIs for tamsulosin
Sulfa allergy
Lowers BP - orthostatic hypotension
Stone passing criteria
Under 5mm - stone will pass
Over 10mm - will not pass
Treatment for stuck kidney stone
Shock wave lithotripsy
- Avoid if may be pregnant
-Focus shockwaves
Ureteroscopic extraction
Percutaneous nephrolithotomy
- 15+mm or bottom of kidney
Prevention for urinary stone disease
Consistent fluid intake
DONT decrease dietary calcium
Things treat calcium stones
Thiazide diuretics help
Cellulose phosphate
Treat hypercalciuria (resorptive or renal)
Hyperoxaluric stones
Some calcium
Often linked to IBD
Avoid vitamin C
Hyperuricosuric stones
Mostly uric acid
Cut back on meat and beer - purines
Alipurinol
Hypercitraturic stones
Due to diarrhea - drink lemonade
Uric acid calculi
Hyperuricemia or abrupt cell death
Low pH and harder to see on X-ray
Potassium citrate or alopurinol
Struvite calculi
P-bacteria - related to UTI
Often staghorn
Proteus, Pseudomonas, Providencia
Cysteine calculi
Often genetic
Give citrate or bicarbonate
Double urine goal for these pts
