Renal/GU Flashcards
(97 cards)
1
Q
Define acute kidney injury.
A
a rapid decline in renal function, with an increase in serum creatine level (relative increase of 50% or absolute increase of 0.5-1.0 mg/dL)
2
Q
What are the RIFLE criteria?
A
a method for stratifying varying degrees of renal dysfunction
- Risk: 1.5 fold increase in serum creatinine, GFR decrease by 25%, or UOP less than 0.5 mL/kg/hr for 6 hours
- Injury: 2-fold increase in serum creatinine, GFR decrease by 50%, or UOP less than 0.5 mL/kg/hr for 12 hours
- Failure: 3-fold increase in serum creatinine, GFR decrease by 75%, or UOP less than 0.5 mL/kg/hr for 24 hours
- Loss: of kidney function requiring dialysis for more than 4 weeks
- ESRD: loss of kidney function requiring dialysis for more than 3 months
3
Q
What would cause an elevated BUN or creatinine apart from AKI?
A
- BUN may be elevated by catabolic drugs such as steroids, GI/soft tissue bleeding, or dietary protein intake
- creatinine may be elevated with increased muscle breakdown and various drugs
4
Q
What is the most common cause of death in those with AKI?
A
infection
5
Q
What happens to BUN/Cr, FENa, and urine osmolality in someone with pre-renal azotemia?
A
- when RBF decreases, BUN reabsorption is enhanced and the BUN/Cr increases > 15
- since tubular function is intact, FENa is normal (<1%) and urine osmolarity is normal (>500 mOsm/kg)
6
Q
What happens to BUN/Cr, FENa, and urine osmolality in someone with post-renal azotemia?
A
- in the early stage, increased tubular pressure enhances BUN reabsorption, and the BUN/Cr increases > 15
- in the early stage, tubular function is also normal with FENa < 1% and urine osmolarity > 500mOsm/kg
- with long-standing obstruction, tubular damage ensues and the BUN/Cr falls, FENa rises, and there is an inability to concentrate urine
7
Q
How is fractional excretion of a solute calculated?
A
FE = (solute excreted)/(solute filtered) = (urine solute)(urine flow rate)/(GFR x plasma solute) = (plasma creatinine x urine solute)/(urine creatinine x plasma solute)
8
Q
Pre-Renal Failure
- causes
- pathogenesis
- presentation
- lab findings
A
- the most common cause of AKI
- due to decreased systemic arterial blood volume or renal perfusion as in hypovolemia, CHF, hypotension, renal arterial obstruction, hepatorenal syndrome, and NSAIDs, ACE inhibitors, and cyclosporin
- in these situations renal blood flow decreases, lowering GFR, which leads to decreased clearance of metabolites like BUN, Cr, and uremic toxins; tubular function is preserved so the kidney conserves sodium and water
- presents with signs of volume depletion
- labs demonstrate oliguria, an increased BUN/Cr ratio greater than 20, increased urine osmolality, and decreased urine sodium with a FENa less than 1%
- UA is likely to demonstrate hyaline casts
9
Q
Name three drugs that may precipitate prerenal failure and through what mechanism they do.
A
- NSAIDs constrict afferent arterioles
- ACE inhibitors cause efferent arteriole vasodilation
- cyclosporin
10
Q
How can labs help you differentiate between prerenal and intrinsic renal failure?
A
- prerenal is likely to have a BUN/Cr ratio greater than 20, FENa less than 1%, high urine osmolality, and low urine sodium
- intrinsic is likely to have a BUN/Cr ratio less than 20, FENa of 1-2%, low urine osmolality, and high urine sodium
11
Q
Intrarenal Failure
- pathogenesis
- causes
- presentation
- laboratory findings
A
- damaged renal parenchyma such that GFR and tubular function are significantly impaired
- may be caused by acute tubular necrosis, glomerular disease, vascular diseases like TTP or HUS, interstitial nephritis
- presentation varies depending on the cause
- lab findings include BUN/Cr ratio less than 20 although both are still elevated in serum, increased urine sodium and decreased urine osmolality
12
Q
Describe how rhabdomyolysis affects the kidneys and how it appears on labs.
A
- skeletal muscle breakdown caused by trauma, crush injuries, prolonged immbolity, snake bites, etc.
- leads to myoglobin released into the blood stream, which is toxic to the kidneys, leading to intrinsic AKI
- presents with elevated creatine phosphokinase, hyperkalemia, hypocalcemia, and hyperuricemia
- treat with IV fluids, mannitol for diuresis, and bicarbonate
13
Q
Postrenal Failure
A
- the least common cause of AKI
- due to an obstruction of any segment of the urinary tract; however, both kidneys must be obstructed for creatinine to rise
- this is most commonly due to BPH; other causes include obstruction of a solitary kidney, nephrolithiasis, obstructing neoplasm
14
Q
Why is post renal failure uncommon?
A
because both kidneys must be obstructed for the creatinine to rise
15
Q
Acute Tubular Necrosis
A
- the most common cause of acute renal failure
- due to ischemia or nephrotoxicity in the form of aminoglycosides, vancomycin, heavy metals, myoglobinuria as in crush injury, ethylene glycol, radio contrast dye, or urate from tumor lysis syndrome, cisplatin, amphotericin, kappa and gamma light chains in multiple myeloma
- injury results in necrosis of tubular epithelial cells, which form brown, granular casts and diminish GFR
- tubular dysfunction leads to elevated BUN and Cr, though the BUN/Cr is < 15, FENa 1-2%, and Osm < 500
- UA likely to find muddy brown casts with trace protein and no blood
- clinical features include oliguria as well as hyperkalemia and acidosis due to the inability to secrete these cations
- reversible but requires supportive dialysis since electrolyte imbalances can be fatal
- recovery takes 2-3 weeks as tubular cells are stable and take time to re-enter the cell cycle
16
Q
What is the workup like for a patient with AKI?
A
- urinalysis
- urine chemistry
- serum electrolytes
- bladder catheterization to rule out obstruction
- renal ultrasound to rule out obstruction
17
Q
What do each of the following suggest when found on urinalysis:
- hyaline casts
- RBC casts
- WBC casts
- fatty casts
A
- hyaline: prerenal failure
- RBC casts: glomerular disease
- WBC casts: renal parenchymal inflammation
- fatty casts: nephrotic syndrome
18
Q
What are the most common mortal complications seen in the early phases of AKI?
A
hyperkalemic cardiac arrest and pulmonary edema
19
Q
What are the possible complications of AKI?
A
- volume expansion resulting in pulmonary edema
- hyperkalemia due to decreased excretion of potassium and the movement of potassium from the ICF to ECF due to tissue destruction and acidosis
- metabolic acidosis with anion gap due to decreased excretion of hydrogen ions
- hypocalcemia due to an inability for form active vitamin D
- hyponatremia if water intake is greater than body losses
- hyperphosphatemia
- hyperuricemia
- uremia
- infection due to impaired immune function secondary to azotemia
20
Q
Acute Kidney Injury
A
- a rapid decline in renal function with an increase in serum creatinine
- can be prerenal (most common), intrarenal, or postrenal (least common)
- prerenal is caused by hypovolemia, low cardiac output, systemic vasodilation, hepatorenal syndrome, or renal artery obstruction; intrarenal by acute tubular necrosis, glomerular disease, or interstitial disease; post renal by an obstruction of both kidneys
- weight gain and edema are the most common presenting symptoms; others include uremia and changes in urine volume
- prerenal shows an elevated BUN/Cr ratio, high urine osmolality, low urine sodium, and low FENa; intrarenal shows lower BUN/Cr, low urine osmolality, high urine sodium, and high FENa
- hyaline casts suggest prerenal failure, muddy brown casts suggest ATN, RBC casts indicate glomerular disease, WBC casts indicate parenchymal inflammation, and fatty casts indicate nephrotic syndrome
- may be complicated by volume expansion and pulmonary edema, hyperkalemia, metabolic acidosis, hypocalcemia, hyponatremia, hyperphosphatemia, hyperuricemia, uremia, and infection
- treat by adjusting medication regimen, stabilizing fluid levels with IVF or diuretics, and correcting electrolyte disturbances
- order dialysis for severe and intractable complications
21
Q
Why does radiographic contrast lead to ATN? How does this affect it’s practical administration?
A
it causes a spasm of the afferent arteriole, which we can prevent with saline hydration before the contrast
22
Q
What is the difference between azotemia and uremia?
A
- azotemia refers to an elevation of BUN
- uremia refers to the signs and symptoms associated with accumulation of nitrogenous wastes due to impaired renal function (usually when BUN is greater than 60)
23
Q
At what point does azotemia typically become symptomatic as uremia?
A
once BUN is greater than 60
24
Q
How is ESRD defined?
A
- not by either BUN or creatinine
- but rather as a loss of kidney function that leads to laboratory and clinical findings of uremia
25
Chronic Kidney Disease
- decreased kidney function (GFR < 60) or kidney damage for at least 3 months
- most commonly caused by diabetes or hypertension; other causes include chronic glomerulonephritis, interstitial nephritis, PKD, and AKI
- presets with hypertension, CHF, volume overload, uremia, normocytic anemia, platelet dysfunction and bleeding, immune dysfunction, hyperphosphatemia causing hypocalcemia and a secondary hyperparathyroidism complicated by renal osteodystrophy and calciphylaxis, hyperkalemia, hypermagnesemia, and metabolic acidosis
- diagnose with a CMP, estimation of GFR, CBC, and renal ultrasound
- symptomatic volume overload and severe hyperkalemia are the complications that require the most urgent treatment
- management involves a low protein diet (0.7-0.8 g/kg); restriction of sodium, magnesium, potassium, and phosphate; ACE inhibitors; glycemic control; calcium citrate as a phosphate binder; oral calcium and vitamin D supplementation; EPO; and dialysis or transplantation
26
Describe the presentation of chronic kidney disease
- hypertension secondary to salt and water retention
- CHF due to volume overload, HTN, and anemia
- uremia: pericarditis, n/v, loss of appetite, restless legs, asterixis, hyperreflexia, altered mental status
- normocytic normochromic anemia secondary to EPO deficiency
- bleeding due to platelet dysfunction as a result of uremia, which prevents platelet degranulation
- hyperphosphatemia due to reduced clearance, decreases 1,25-OH vitamin D production, leads to hypocalcemia, causing secondary hyperparathyroidism, manifesting as renal osteodystrophy, and fractures
- calciphylaxis as calcium and phosphate precipitate causing vascular calcifications and then necrotic skin lesions
- decreased testosterone in men; amenorrhea, infertility, and hyperprolacitinemia in women
- volume overload with pulmonary edema
- hyperkalemia, hypermagnesemia, metabolic acidosis
- immune dysfunction
27
What is renal insufficiency?
a term used when a patient's renal function is irreversibly compromised by not failed
28
Why are ACE inhibitors important in the treatment of chronic kidney disease?
- because it dilates the efferent arteriole of the glomerulus, slowing the progression of proteinuria
- it also helps control blood pressure, which slows disease progression
29
What are the indications for dialysis?
AEIOU
- Acidosis (intractable)
- Electrolytes (severe, persistent hyperkalemia)
- Intoxications (with methanol, ethylene glycol, lithium, or aspirin)
- Overload (volume not manageable with other means)
- Uremia (severe)
30
Describe the process of and the pros and cons related to hemodialysis as opposed to peritoneal dialysis.
- patient's blood is heparinized and then passed through the dialyzer for 3-5 hours, 3 days per week
- access is obtained with a central catheter, tunnel catheter, AV fistula, or implantable graft
- more efficient and can be initiated more quickly than peritoneal dialysis
- however, it is less similar to the normal physiology of the kidney so there is a greater risk of hypotension or hypoosmolality during the process
31
What is the advantage of continuous arteriovenous hemodialysis and continuous venovenous hemodialysis?
they use lower flower rates than traditional hemodialysis, which minimizes any rapid shifts in volume or osmolality, making it a good option for hemodynamically unstable patients
32
Describe the process of and the pros and cons related to peritoneal dialysis as opposed to hemodialysis.
- the peritoneum serves as the dialysis membrane with a dialysate fluid infused into the peritoneal cavity
- the fluid must be drained and replaced every hour in an acute setting but once every 4-8 hours thereafter
- advantageous in that patients can learn to do it on their own
- the dialysate fluid has a high glucose load which can contribute to hyperglycemia, it is a risk factor for peritonitis, it increases intraabdominal pressure posing a risk for inguinal or abdominal hernia, it increases abdominal girth so it has some cosmetic disadvantages
33
How do we define proteinuria?
as urinary excretion of more than 150mg protein/day
34
How do glomerular, tubular, and overflow proteinuria compare with one another in cause ?
- glomerular is due to increased glomerular permeability to proteins and protein loss tends to be more severe
- tubular is due to decreased tubular reabsorption of the smaller proteins which are normally filtered through the glomerulus due to sickle cell disease, urinary tract obstruction, or interstitial nephritis
- overflow proteinuria is caused by increased production of small proteins which overwhelm the tubules' ability to reabsorb them (i.e. Bence Jones protein in multiple myeloma)
35
Describe nephrotic syndrome.
- defined by urine protein excretion greater than 3.5g/day
- presents with hypoalbuminemia and resulting edema
- hyperlipidemia in the form of elevated LDL and VLDL as the liver attempts to increase albumin synthesis
- increased risk fo infection as immunoglobulins are lost
- hypercoagulable state as antithrombin III is lost
36
Describe nephritic syndrome.
changes due to inflammation of the glomeruli
- proteinuria is limited (< 3.5 g/day)
- oliguria and azotemia, signs of AKI
- salt retention with periorbital edema and hypertension
- RBC casts
37
Urine dipstick is capable of detecting what types and amounts of protein?
- detects concentrations 30mg/dL or higher (won't detect microalbuminuria)
- more sensitive to albumin than immunoglobulins
38
How should microalbuminuria be diagnosed?
- defined as albumin excretion of 30-300mg/day, which is below the sensitivity of a dipstick
- special dipsticks are required to screen for microalbuminuria and should then be confirmed with a radioimmunoassay
39
What do nitrite and leukocyte esterase in a UA suggest?
- nitrites suggest the presence of bacteria in urine
| - leukocyte esterase suggests the presence of WBC in urine
40
How should proteinuria be treated?
if it is transient, no further workup or treatment is needed; otherwise symptomatic proteinuria requires:
- ACE inhibitors to slow albumin loss
- diuretics to treat edema
- dietary protein and sodium restriction
- lipid-lowering agents
41
Proteinuria
- defined as urinary excretion of more than 150 mg/day
- can be classified as glomerular, which is most severe; tubular in which small proteins that are filtered are not absorbed; or overflow in which production of small proteins overwhelms the tubules' reabsorbative abilities
- nephrotic syndrome is a specific subset defined by more than 3.5g/day of protein loss; characterized by edema, hyperlipidemia, hypercoagulable state, and risk of infection
- urine dipstick and urinalysis are important for diagnosis and evaluation
- treatment involves ACE inhibitors, diuretics, dietary protein and sodium restriction, and lipid-lowering agents if symptomatic and not transient
42
Hematuria
- defined as more than 3 RBCs/HPF on urinalysis
- microscopic tends to be glomerular in origin while gross hematuria is more commonly urologic in origin
- infection and kidney stones cause most cases; bladder or kidney cancer, glomerular diseases such as IgA nephropathy, and trauma are possible causes
- diagnosed with dipstick and urinalysis; should be followed up with a urine specimen for cytology to rule out malignancy
43
Gross, painless hematuria should be considered evidence of what until proven otherwise?
should be considered a sign of bladder or kidney cancer until proven otherwise
44
What should be done following discovery of hematuria?
collect a urine specimen for cytology in order to exclude kidney or bladder cancer before evaluating for other causes
45
Minimal Change Disease
- the most common cause of nephrotic syndrome in children
- usually idiopathic, but may be associated with lymphoma
- glomeruli appear normal on light microscopy, but effacement of foot processes can be seen on EM
- proteinuria is selective (only albumin)
- respond extremely well to steroids
46
Focal Segmental Glomerulosclerosis
- the most common cause of nephrotic syndrome in Hispanics and African Americans
- often idiopathic but may be associated HIV, IV drug use, or sickle cell disease
- sclerosis involving part of some glomeruli is visible on light microscopy and effacement of foot processes can be seen on EM
- doesn't respond well to steroids and progresses to renal insufficiency within 5-10 years
47
Membranous Glomerulonephritis
- the most common cause of nephrotic syndrome in Caucasian adults
- usually idiopathic but may be associated with HBV, HCV, solid tumors, or SLE
- light microscopy reveals thickened glomerular basement membranes, IF shows granular immune complex deposits, and EM shows sub epithelial deposits
48
Diabetic Glomerulonephropathy
- nonenzymptic glycosylation of the vascular basement membrane results in hyaline arteriolosclerosis, reducing lumen diameter
- efferent arteriole more affected than afferent, increasing the GFR, and this hyperfiltration injury leads to microalbuminuria
- eventually progresses to nephrotic syndrome characterized by sclerosis of the mesangium with formation of Kimmelstiel-Wilson nodules
- ACE inhibitors slow the progression by inhibiting efferent arteriolar constriction
49
Alport Syndrome
- an X-linked dominant type IV collagen defect
- results in thinning and splitting of the glomerular basement membrane
- presents with hematuria, sensory hearing loss, and ocular disturbances
50
Membranoproliferative Glomerulonephritis
- a mix of nephritic and nephrotic syndrome
- type I is characterized by subendothelial deposits and an associated with HBV and HCV
- type II is characterized by intramembranous, "ribbon-like" deposits and C3 nephrotic factor (an antibody that stabilizes C3 convertase; see low levels of C3 in patient)
- light microscopy reveals a "tram-track" appearance
- IF reveals granular immune complex deposition
51
IgA Nephropathy
- the most common cause of glomerular hematuria worldwide
- it is due to IgA complex deposition in the mesangium
- presents during childhood with episodic hematuria with RBC casts present in urine, typically following mucosal infections; renal function is usually normal
- it is the renal pathology of Henoch-Schonlein purpura
52
Pststreptococcal Glomerulonephritis
- also known as acute proliferative glomerulonephritis
- a nephritic syndrome arising 2-3 weeks after a group A, beta-hemolytic strep infection
- glomeruli appear hypercellular
- granular, subepithelial deposits of IgG, IgM, and C3
- treatment is supportive as children rarely progress to renal failure; adults more likely to develop RPGN
53
Rapidly Progressive Glomerulonephritis
- a nephritic syndrome that progress to renal failure in weeks to months
- a description, not a disease
- cases are split into three groups (anti-GBM disease, RPGN related to systemic disease, and Pauli-Immune type) based on the pattern of immunofluorescence and other features
- all share the light microscope finding of crescents in Bowman space comprised of fibrin and macrophages
54
Goodpasture Syndrome
- a type of RPGN known as goodpasture syndrome
- a type II hypersensitivity mediated by antibodies directed against the basement membrane of alveoli and glomeruli
- most common in males between 20-40 with hemoptysis preceding hematuria
- strongly associated with the HLA-DR2 haplotype
- light microscopy finds hyper cellular glomeruli surrounded by a fibrin/macrophage crescent
- immunofluorescence confirms a linear pattern of IgG and C3
- treat with plasmapheresis, cyclophosphamide, and steroids
55
Diffuse Proliferative Glomerulonephritis
- a type of RPGN secondary to systemic disease; in particular it is the most common type of renal disease seen in patients with SLE
- mediated by antigen-antibody complex deposition
- light microscope finds hyper-cellular glomeruli surrounded by a fibrin/macrophage crescent and "wire looping" of capillaries
- IF confirms granular complex deposits of IgG and C3 and EM finds sub-endothelial deposits
56
Pauci-Immune Proliferative Glomerulonephritis
- a type of RPGN associated with various types of vasculitis, particularly Wegener granulomatosis, polyangiitis, and Churg-Strauss syndrome
- IF is negative but ANCA (anti-neutrophil cytoplasmic antibodies) are present in serum; c-ANCA for wegener granulomatosis and p-ANCA for Churg-Strauss
- light microscopy finds hyper-cellular glomeruli surrounded by a fibrin/macrophage crescent
57
Acute Interstitial Nephritis
- an intra-renal azotemia
- characterized as a drug-induced hypersensitivity affecting the interstitium and tubules
- most commonly due to the 5 P's: Pee (diuretics), Pain-free (NSAIDS), Penicillins, Proton pump inhibitors, and rifamPin
- presents with oliguria, fever, and rash lasting days to weeks
- uniquely, there is eosinophilia and eosinophils present in the urine; there may also be some degree of pyuria, hematuria, and proteinuria
- removing the offending agent and steroids are the preferred treatment
- may progress to renal papillary necrosis
58
Renal Papillary Necrosis
- necrosis of renal papillae
- due to chronic analgesic abuse, diabetes mellitus, sickle cell disease/trait, severe acute pyelonephritis, or renal transplant
- the diagnosis is made by excretory urogram
- presents with gross hematuria and flank pain
- sloughed material may lead to ureteral obstruction
59
What is renal tubular acidosis?
it is a disorder of the renal tubules that leads to a non-anion gap hyperchloremic metabolic acidosis in the setting of normal glomerular functioning
60
Type I Renal Tubular Acidosis
- an inability to secrete protons at the distal tubules, which prevents new bicarbonate from being generated
- causes include congenital obstruction, multiple myeloma, autoimmune diseases, amphotericin B toxicity, and analgesic nephropathy
- urine pH is greater than 5.5, there is a decrease in ECF volume, there is a hypokalemia, and there is a hyperchloremic, nonunion gap metabolic acidosis
- notably, renal stones often form; rickets/osteomalacia are another possible complication
- treat with sodium bicarb and phosphate salts which promote excretion of acid
61
Type II Renal Tubular Acidosis
- an inability to reabsorb bicarb at the proximal tubule
- causes include Fanconi syndrome, multiple myeloma, carbonic anhydrase inhibitors
- the urine pH will be less than 5.5, there is hypokalemia, sodium is also lost in the urine, and nephrolithiasis does not occur
- treatment involves sodium restriction as this increases sodium reabsorption and thus bicarb reabsorption in the proximal tubules; any bicarb administered will just be excreted in the urine
62
Type IV Renal Tubular Acidosis
- decreased sodium absorption and decreased proton and potassium secretion in the distal tubule
- caused by any condition associated with hypoaldosteronism or renal resistance to aldosterone such as ACE inhibitor, potassium sparing diuretic, or NSAIDs use
- common in those with interstitial renal disease or diabetic nephropathy
- the urine pH will be less than 5.5 and there is a hyperkalemia
63
List the different causes and features of the three types of tubular acidoses.
- 1: inability to secrete protons in the distal tubule; caused by congenital obstruction, multiple myeloma, analgesic nephropathy, amphotericin B, and autoimmune diseases; leads to hypokalemia, urine pH more than 5.5, and renal stones
- 2: inability to reabsorb bicarb in the proximal tubule; caused by multiple myeloma, carbonic anhydrase inhibitors, and Fanconi syndrome; leads to hypokalemia, urine pH less than 5.5, and no renal stones
- 4: decreased sodium absorption and decreased proton and potassium secretion in the distal tubule; caused by hypoaldosteronism and common in those with interstitial renal disease or diabetic nephropathy; leads to hyperkalemia, urine pH less than 5.5
64
What is Hartnup syndrome?
- an autosomal recessive defect in amino acid transport
- results in decreased intestinal and renal reabsorption of neutral amino acids, including tryptophan, which causes a nicotinamide deficiency
- presents with dermatitis, diarrhea, ataxia, and psych disturbances
- treat by supplementing nicotinamide
65
What is Fanconi syndrome?
- a tubular defect which limits reabsorption of all solutes from the proximal tubule
- can be acquired or hereditary
- associated with glycosuria, phosphaturia and skeletal problems, proteinuria, polyuria, dehydration, type 2 RTA, hypercalciuria, and hypokalemia
- treat with phosphate, potassium, alkali and salt supplementation, and adequate hydration
66
Autosomal Dominant PKD
- an inherited defect leading to bilaterally enlarged kidneys with cysts in the renal cortex and medulla
- presents with hematuria, abdominal pain, hypertension, and palpable kidneys
- renal failure eventually occurs from recurrent pyelonephritis and nephrolithiasis
- associated with intracerebral berry aneurysms, mitral valve prolapse, and hepatic cysts
- diagnose with ultrasound
- treatment involves draining symptomatic cysts, controlling hypertension, and treating infections
67
Autosomal Recessive PKD
- an inherited defect leading to bilaterally enlarged kidneys with cysts in the renal cortex and medulla
- presents in infants as worsening renal failure with hypertension, abdominal distention, and possibly Potter sequence
- associated with congenital hepatic fibrosis, leading to portal hypertension, hepatic cysts, and cholangitis
- treat by managing respiratory issues and with renal transplant
68
Medullary Cystic Kidney Disease
- an autosomal dominant condition resulting in the cystic dilation of the collecting ducts
- presents with hematuria, UTIs, or nephrolithiasis
- associated with hyperparathyroidism and parathyroid adenoma
- diagnosed by IVP
- treat with stone prevention and management of recurrent UTIs
69
Describe the pathogenesis of renovascular hypertension.
decreased blood flow to the juxtaglomerular apparatus causes the renin-angiotensin-aldosterone system to become activated, which contributes to hypertension
70
What is the most common cause of secondary hypertension?
renal artery stenosis
71
What are the two primary causes of renal artery stenosis and how do the two compare?
- atherosclerosis is more common, but typically affects elderly men with a history of smoking or high cholesterol levels
- fibromuscular dysplasia more often affects young females and is more often bilateral
72
Describe the presentation of renal artery stenosis.
- severe hypertension refractory to medical therapy
- decreased renal function
- abdominal bruit is often present
73
How is renal artery stenosis diagnosed?
- renal arteriogram is the gold standard but the dye used can be nephrotoxic and should be avoided in those with renal failure
- magnetic renal arteriogram is the new test, which uses magnetic dye that is not nephrotoxic
74
Renal Artery Stenosis
- a narrowing of the renal arteries
- can be due to atherosclerosis (more common in elderly men with history of smoking or high cholesterol) or to fibromuscular dysplasia (more common in young women)
- decreased blood flow to the JGA activates the renin-angiotensin-aldosterone system
- presents with severe, refractory hypertension, decreased renal function, and abdominal bruit
- diagnosed using a renal arteriogram
- treat with some combination of ACE inhibitors, calcium channel blockers, and revascularization
75
Benign Nephrosclerosis
- a thickening of the glomerular afferent arterioles which develops in those with long-standing hypertension
- because hypertension increases capillary hydrostatic pressure in the glomeruli, which leads to sclerosis
- labs find mild to moderate increases in creatinine, microscopic hematuria, and mild proteinuria
- treat with blood pressure control
76
How does malignant nephrosclerosis differ from benign nephrosclerosis?
- in this case, the sclerosis leads to a rapid decrease in renal function and an accelerated hypertension
- labs differ in that BP is more elevated, potentially with CNS findings such as papilledema; creatine rises, hematuria, proteinuria, RBC and WBC casts occur more rapidly
77
Describe sickle cell nephropathy.
- pathogenesis involves sickling in the renal microvasculature, which leads to infarction, mostly in the renal papilla
- this can lead to papillary necrosis, renal failure, a high frequency of UTIs, and possibly nephrotic syndrome
- additionally ischemic injury to the renal tubules can occur, which increases the risk for dehydration, which precipitates further sickling
- treatment is usually with ACE inhibitors
78
Where are obstructing nephrolithiases most likely to be seen?
the ureterovesicular junction or intersection of the ureter and the iliac vessels near the pelvic brim
79
What would contribute to hypercalciuria and the formation of calcium stones?
primary hyperparathyroidism, sarcoidosis, malignancy, vitamin D excess, etc.
80
What is unique about calcium stones?
- they are the most common type of renal stone
- they form secondary to hypercalciuria (due to primary hyperparathyroidism, sarcoidosis, malignancy, vitamin D excess) or hyperoxaluria (due to severe steatorrhea, small bowel disease, or pyridoxine deficiency)
- they are radiodense and have an envelope shape on microscopy
- the treatment is HCTZ, a calcium sparing diuretic
81
What is unique about uric acid stones?
- risk factors include acidic urine, low urine volume, and hot, arid climates
- associated with gout and myeloproliferative disorders
- the stones are radiolucent and crystals are rhomboid in shape
- treatment involves hydration, alkalinization of urine, and allopurinol
82
What is unique about struvite stones?
- usually due to infection with a urease-positive organism like proteus or klebsiella, so alkaline urine is a risk factor
- they are radiodense and form stag horn calculi
- crystals are coffin-lid shaped
- requires surgical removal
83
What is unique about cystine stones?
- typically presents in childhood-
- associated with cystinuria, a genetic tubule defect resulting in poor cysteine reabsorption as well as poor reabsorption of ornithine, lysine, and arginine
- the urine crystals are hexagonal
- treatment involves hydration and alkalinization of urine
84
How do renal stones present?
- sudden, severe pain that occurs in waves and radiates from the flank toward the groin
- nausea and vomiting are common
- hematuria
85
What is the initial test for locating renal stones and what is the gold standard?
- a plain radiograph is the initial test
| - CT scan is the gold standard and can detect even stones that are radiolucent on a KUB
86
How are renal stones treated?
- analgesia, fluid hydration, and antibiotics if there is a UTI present
- if pain is severe, especially with vomiting, obtain a KUB and an IVP to find the site of obstruction
- stones less than 0.5 cm are likely to pass on their own; consult urology if the stone has not passed after three days
- urology will likely perform lithotripsy or surgery depending on the size of the stone
87
Which stones are amenable to lithotripsy and which require surgery?
- stones less than 0.5 cm are likely to pass on their own
- those 0.5-2.0 cm are amenable to lithotripsy
- those larger than 2 cm often require percutaneous nephrolithotomy
88
Renal Cell Carcinoma
- a malignant epithelial tumor arising from the tubules
- risk factors include cigarette smoking, phenacetin analgesics, ADPKD, chronic dialysis, heavy metal exposure, hypertension, and VHL syndrome
- presents with a triad of hematuria, palpable mass, and abdominal or flank pain
- paraneoplasic syndromes derived from increased EPO, renin, PTHrP, or ACTH (polycythemia vera, HTN, hypercalcemia, or Cushing syndrome)
- most likely to metastasize to the lungs or bone
- diagnose with a renal ultrasound or abdominal CT
- treat with radical nephrectomy
89
Bladder Cancer
- most cases are transitional cell carcinomas, which can arise anywhere from the kidney to the bladder
- risk factors include cigarette smoking, industrial carcinogen exposure, and long-term treatment with cyclophosphamide
- presents with painless hematuria and urinary symptoms
- diagnosed based on UA and urine culture to rule out infection, urine cytology, cystoscopy with biopsy, and chest CT for staging
- treatment depends on the stage of the disease; but if resected, it is likely to recur, so frequent cystoscopy is recommended in follow-up
90
What is the most important risk factor for prostate cancer?
age
91
Prostate Adenocarcinoma
- a malignant proliferation of prostatic glands
- risk factors include age, race (AA most and Asians least), and a diet high in saturated fats
- most often, it is clinically silent as it arises in the peripheral, posterior region and does not affect the ureter until late; later patients may have symptoms of difficulty voiding, dysuria, urinary frequency, weight loss, and bone pain from metastases
- initial evaluation involves a digital rectal exam and PSA, followed by a transrectal ultrasound and biopsy if PSA is greater than 10, PSA velocity is greater than 0.75, or the DRE is abnormal
- treatment options include radiation, androgen deprivation, and radical prostatectomy
92
What are the indications for transrectal ultrasonography with biopsy in those with suspected prostate adenocarcinoma?
- should be performed if PSA is greater than 10
- if PSA velocity is greater than 0.75 per year
- if the digital rectal examination is abnormal
93
What are potential causes of elevated PSA?
prostatic massage, needle biopsy, cystoscopy, BPH, prostatitis, and advanced age
94
What kind of PSA is more specific for prostate adenocarcinoma?
protein-bound PSA
95
Describe the treatment for prostate adenocarcinoma.
- radical prostatectomy is the definitive therapy for localized disease, but may lead to ED or urinary incontinence and are avoided in those with a life expectance less than 10 years
- radiation therapy plus androgen deprivation are the other options for locally invasive and metastatic disease, with orchiectomy, anti androgens, leuprolide, and GnRH antagonists
96
Testicular Torsion
- a twisting of the spermatic cord
- causes the thin-walled veins to collapse while the arteries remain open, resulting in congestion and hemorrhage infarction
- usually due to congenital failure of the testes to attach to the inner lining of the scrotum via the processes vaginalis
- presents in adolescents with sudden testicular pain, an absent cremasteric reflex, swollen and tender scrotum, and an elevated testicle
- treat with surgical detorsion and orchiopexy to the scrotum bilaterally within 6 hours
97
What are the organisms most commonly responsible for epididymitis and prostatitis?
- E. coli in older men and children
| - gonorrhea and chlamydia in younger men
