Step Up - Diseases of the Renal and Genitourinary System Flashcards
AKI is also called?
ARF - Acute renal failure.
Types of AKI:
Prerenal - Decrease in renal blood flow (60-70% of cases).
Intrinsic - Damage to renal parenchyma (25-40% of cases).
Postrenal - Urinary tract obstruction (5-10% of cases).
AKI is oliguric, anuric, or nonoliguric?
It can be either. Severe AKI may occur without a reduction of urine output.
Most common clinical findings in patients with AKI?
Weight gain + edema - This is due to a positive water and Na balance.
AKI is characterized by?
Azotemia - elevated BUN + Cr.
Elevated BUN is also seen with?
Catabolic drugs (eg steroids), GI/soft tissue bleeding, and dietary protein intake.
Elevated Cr is also seen with?
Incr. muscle breakdown and various drugs. Baseline Cr level varies proporptionately with muscle mass.
Prognosis of AKI:
> 80% recover completely. However, the prognosis varies widely depending on the severity of renal failure and the presence of comorbid conditions.
MCC of death in AKI?
Infection - 75%. Followed by cardiorespiratory complications.
MCC of AKI?
Prerenal failure - potentially reversible.
What drugs should NOT be given in patients with decr. renal perfusion?
- NSAIDs (constrict afferent arteriole).
- ACEIs (vasodilate efferent arteriole).
- Cyclosporin.
ALL can precipitate prerenal failure.
Monitoring a patient with AKI:
- Daily weights, intake, and output.
- BP.
- Serum electrolytes.
- Watch Hb and Hct for anemia.
- Watch for infection.
Diagnostic approach in AKI:
- History + Physical exam.
- 1st thing to do is to determine the DURATION of renal failure –> Baseline Cr.
- 2nd thing is to determine whether AKI is due to prerenal, intrarenal, and postrenal causes –> Combine history, physical exam, lab findings.
- Medication review.
- Urinanalysis.
- Urine chemistry (FENa, osmolarity, urine Na, urine Cr).
- Renal US - To rule out obstruction.
Prerenal vs ATN - Urine osmolarity:
Prerenal - >500.
ATN - >350.
Prerenal vs ATN - Urine Na:
Prerenal: 40.
Prerenal vs ATN - FENa:
Prerenal: 1%.
Prerenal vs ATN - Urine sediment:
Prerenal: Scant.
ATN: Full, brownish pigment, granular casts with epithelial casts.
Studies to differentiate prerenal from intrinsic AKI - Urinanalysis:
Prerenal: Hyaline casts.
Intrinsic: Abnormal.
Studies to differentiate prerenal from renal AKI - BUN/Cr:
Prerenal –> >20:1.
Renal –> <20:1.
Studies to differentiate prerenal from renal AKI - FENa:
Prerenal –> >2-3%.
Studies to differentiate prerenal from renal AKI - Urine osmolarity:
Prerenal: >500mOsm.
Renal: 250-300mOsm.
Studies to differentiate prerenal from renal AKI - Urine sodium:
Prerenal –> >40.
Prerenal failure - Why Oliguria ALWAYS?
To preserve volume.
Prerenal failure - Why BUN-to-serum Cr >20:1?
Because kidneys can reabsorb urea.
Prerenal failure - Incr. urine osmolarity?
> 500, because the kidneys are able to reabsorb water.
Prerenal failure - Decr. urine Na?
Because Na is avidly reabsorbed.
Prerenal failure - Incr. urine-plasma Cr ratio (>40:1)?
Because much of the filtrate is reabsorbed (but not the Cr.).
MCC of ATN?
Ischemia.
Rhabdomyolysis - Etiology:
Caused by trauma, crush injuries, prolonged immobility, seizures, snake bites.
Rhabdomyolysis - Problem with the kidneys?
Release of muscle fibers contents (myoglobin) into bloodstream –> Toxic to the kidneys, which can lead to AKI.
Rhabdomyolysis - Lab:
- Include markedly elevated CPK.
- Hyperkalemia.
- Hypocalcemia.
- Hyperuricemia.
Rhabdomyolysis - Treatment:
- IV fluids.
- Mannitol (osmotic diuretic).
- Bicarbonate (drives K back into cells).
ATN in multiple myeloma?
From kappa and lamda light chains.
Intrinsic renal failure - BUN/Cr closer to 10:1?
Both are still elevated, but LESS UREA IS REABSORBED than in prerenal failure.
Intrinsic renal failure - Incr. urine Na (FENa >2%-3%)?
Na is poorly reabsorbed.
Intrinsic renal failure - Decr. urine osmolarity (<350)?
Because renal water reabsorption is impaired.
Intrinsic renal failure - Decr. urine-plasma Cr ratio (<20:1)?
Because filtrate cannot be reabsorbed.
Least common cause of AKI?
Postrenal failure.
Post renal failure - What is essential to take place for Cr to rise?
BOTH kidneys must be obstructed for Cr to rise.
Post renal obstruction if untreated, can lead to?
ATN
Post renal failure - etiology:
- Urethral obstruction secondary to BPH - MCC.
- Obstruction of solitary kidney.
- Nephrolithiasis.
- Obstructing neoplasm (bladder, cervix, prostate, and so on).
- Retroperitoneal fibrosis.
- Ureteral obstruction is an uncommon cause, because it needs to be bilateral.
3 basic tests for post renal failure:
- Physical exam –> Palpate the bladder.
- US –> Look for obstruction, hydronephrosis.
- Catheter –> Look for large volume of urine.
How is diagnosis of AKI usually made?
By finding elevated Cr and BUN. Patient is usually ASYMPTOMATIC.
Course of ATN:
- Onset (insult).
- Oliguric phase.
- Diuretic phase.
- Recovery phase.
Oliguric phase of ATN:
- Azotemia and uremia - 10-14d.
2. Urine output <400-500mL/d.
Diuretic phase of ATN:
- Begins when urine output is >500mL/d.
- High urine output due to the following:
a. Fluid overload (excretion of retained salt, water, other solutes that were retained during oliguric phase).
b. Osmotic diuresis due to retained solutes during oliguric phase.
c. Tubular cell damage - delayed recovery of epithelial cell function relative to GFR.
Obtain the following in any patient with AKI:
- Urinanalysis.
- Urine chemistry.
- Serum electrolytes.
- CBC.
- Bladder catheterization to rule out obstruction - diagn. + therapeut.
- Renal US to look for obstruction.
Microscopic exam of the urine sediment - Hyaline casts:
Devoid of contents - seen in prerenal failure.
Microscopic exam of the urine sediment - RBC and WBC casts:
RBC casts –> Glomerular disease.
WBC casts –> Renal parenchymal infl.
Microscopic exam of the urine sediment - Fatty casts:
Nephrotic syndrome.
ATN - Urine sediment:
- Muddy brown casts.
- Renal tubular cells/casts.
- Granular casts.
ATN - Protein and blood in urine?
Protein –> Trace.
Blood –> No.
Acute GN - Urine sediment:
- Dysmorphic RBCs.
- RBCs with casts.
- WBCs with casts.
- Fatty casts.
Acute GN - Protein and blood:
Protein –> 4+.
Blood –> 3+.
Acute interstitial nephritis - Urine sediment:
- RBCs.
- WBCs.
- WBCs with casts.
- Eosinophils.
Acute interstitial nephritis - Protein and blood:
Protein –> 1+.
Blood –> 2+.
Post renal - urine sediment:
- Benign.
- May or may not see RBCs.
- WBCs.
Post renal - Protein and blood:
Protein –> No.
Blood –> No.
Urine Na depends on?
Dietary intake.
FENa:
Prerenal.
2-3% –> ATN.
When FENa is most useful:
If OLIGURIA is present.
What is the renal failure index 5?
UNa/(UCr/UpCr) x 100.
Prerenal failure.
>1% –> ATN.
CT scan role in diagnosis of AKI:
CT abdomen and pelvis - may be helpful - usually done if US shows an abnormality, such as hydronephrosis.
Renal biopsy in diagnosis of AKI:
Usually done if there is suspicion of acute GN or acute allergic interstitial nephritis.
Renal arteriography in diagnosis of AKI:
For possible renal artery occlusion - should be performed only if specific therapy will make a difference.
What types of AKI should be excluded first in the course of diagnosis?
In evaluating a patient with AKI, first exclude PRE- and POST-renal causes, and then, if necessary, investigate intrinsic renal causes.
In the EARLY phase of AKI, the MC mortal complications are:
- Hyperkalemic cardiac arrest.
2. Pulmonary edema.
AKI - Why hyperkalemia?
Due to:
- Decr. excretion of K.
- Movement of K from ICF to ECF due to tissue destruction and acidosis.
AKI - Why metabolic acidosis with incr. anion gap?
Due to:
1. Decr. excretion of H.
If severe (<16mEq/L), correct with HCO3.
AKI - Hypocalcemia?
Loss of ability to form active vitD + rapid development of PTH resistance.
AKI - Hyponatremia?
May occur if water intake is greater than body losses, or if a volume-depleted patient consumes excessive hypotonic solutions.
HYPERnatremia may also be seen in hypovolemic states.
AKI - Hyper- or Hypophosphatemia?
HYPER
AKI - Infection?
A COMMON + SERIOUS complication - 50-60% of cases.
Cause –> Multifactorial, but UREMIA is thought to impair immune functions.
AKI - Treatment - General measures:
- Avoid medications that decr. RBF (NSAIDs) and/or are nephrotoxic (aminoglycosides, radiocontrast agents).
- Adjust medication dosages for level of renal function.
- Correct fluid imbalance.
- Correct electrolyte disturbances if present.
- Optimize CO. BP should be 120-140/80-90.
AKI - Treatment - When to order dialysis:
- If symptomatic uremia.
- Intractable acidemia.
- Hyperkalemia.
- Volume overload
Radiographic contrast media can cause?
ATN –> Typically very rapidly, by causing spasm of the afferent arteriole.
It can be prevented with saline hydration.
Whenever a patient has elevated Cr levels, the 1st thing to do is?
Determine the patient’s BASELINE Cr levels, if possible.
This helps determine whether the patient has AKI, CKD, or chronic renal insufficiency/failure with superimposed AKI (“acute on chronic” renal failure).
CKD is defined:
As either decr. kidney function (GFR<60) or kidney damage (structural/functional abnormalities) for AT LEAST 3 MONTHS regardless of cause.
CKD - Etiology:
- DM - MCC (30%).
- HTN - 25%.
- Chronic GN - 15%.
- Interstitial nephritis.
- PKD.
- Obstructive uropathy.
Azotemia refers?
To elevated BUN.
Uremia refers?
To the signs and symptoms associated with accumulation of nitrogenous wastes due to impaired renal function.
Difficult to predict when uremic symptoms will appear, but it rarely occurs unless the BUN is >60mg/dL.
ESRD is defined?
It is a loss of kidney function that leads to lab and clinical findings of uremia.
It is NOT defined by BUN and Cr levels.
CKD - Clinical features - CVS:
- HTN
- CHF
- Pericarditis (uremic)
CKD - Clinical features - GI:
Usually due to uremia:
- Nausea, vomiting.
- Loss of appetite (anorexia).
CKD - Clinical features - Neurologic:
- Lethargy, confusion, peripheral neuropathy, uremic seizures.
- Weakness, asterixis, hyperreflexia.
- Hypocalcemia –> lethargy, confusion, tetany.
CKD - Clinical features - Hematologic:
- Normocytic normochromic anemia - may be severe.
2. Bleeding secondary to platelet dysfunction - due to uremia. - Platelets do NOT degranulate in a uremic environment.
CKD - Clinical features - Endocrine/metabolic:
- Ca-Ph disturbances –> Hyper Ph –> Decr. renal prod. of vitD –> HypoCa –> 2o HyperPTH.
- In the long run –> HYPERcalcemia may be seen.
- Sexual/reproductive symptoms.
- Pruritus - Common and difficult to treat.
Renal osteodystrophy?
Hypocalcemia leads to secondary hyperPTH, which removes Ca from the bones, making them weak and susceptible to fracture.
CKD - Clinical features - Fluid and electrolyte problems:
- Volume overload - watch for pulm. edema.
- HyperK - decr. secretion.
- HyperMg - 2o to reduced urinary loss.
- HyperPh.
- Met. acidosis - due to loss of renal mass (thus decr. ammonia production) and the kidney’s inability to excrete H.
CKD - Clinical features - Immunologic:
Uremia –> Inhibits cellular and humoral immunity.
Diagnosis of CKD:
- Urinanalysis - Examine sediment.
- Measure Cr clearance to estimate GFR.
- CBC - Anemia, thrombocytopenia.
- Serum electrolytes.
- Renal US - Evaluate SIZE of kidneys/rule out obstruction.
Does presence of normal or large sized kidneys exclude CKD?
No.
In patients with CKD, the MC complications that require urgent intervention are?
- Symptomatic volume overload.
2. Severe hyperkalemia.
Life-threatening complications in CKD:
- Hyperkalemia –> Obtain an ECG.
- Pulmonary edema –> Look for recent weight gain.
- Infection.
CKD Treatment - Diet:
- Low protein.
- Low salt diet if HTN, CHF, or oliguria are present.
- Restrict K, Ph, Mg intake.
CKD Treatment - ACEIs:
Dilate efferent arteriole of glomerulus:
- If used early on, they reduce the risk of progression to ESRD because they slow the progression of proteinuria.
- Use with great caution because they can cause HYPERKALEMIA.
CKD Treatment - BP control:
- Strict control decreases the rate of disease progression.
2. ACEIs are the preferred agents. Diuretics may be required.
CKD Treatment - Correction of electrolytes:
- Correct hyperPh –> With Ca citrate (a phosphate binder).
- Long term Ca + vitD –> Prevent 2o hyperPTH and uremic osteodystrophy.
- Acidosis –> Treat the underlying cause (renal failure) - Patients may require oral HCO3.
CKD Treatment - Pruritus:
Try capsaicin cream or cholestyramine and UV light.
CKD Treatment - What is the only cure?
Transplantation
2 major methods of dialyzing a patient:
- Hemodialysis
2. Peritoneal dialysis
Settings in which dialysis is considered:
- CKD.
- AKI.
- Overdose of medications or ingestions of substances cleared by the kidneys.
Absolute indications for dialysis:
- Acidosis
- Electrolytes - Severe hyperkalemia.
- Intoxications - methanol, ethylene glycol.
- Overload - hypovolemia not managed by other means.
- Uremia (severe) - based on clinical presentation, not lab values - eg uremic pericarditis.
Specific indications for dialysis - Nonemergent indications:
- Cr and BUN are NOT absolute indications for dialysis.
- Symptoms of uremia:
a. Nausea, vomiting.
b. Lethargy/deterioration in mental status.
c. Encephalopathy.
d. Seizures.
e. Pericarditis.
Specific indications for dialysis - Emergent indications:
- Life-threatening manifestations of volume overload - Pulm. edema, HTN emergency.
- Severe, refractory electrolyte disturbances.
- Severe metabolic acidosis.
- Drug toxicity/ingestions.
Dialyzable substances:
- Salicylic acid
- Lithium
- Ethylene glycol
- Mg-containing laxatives
Frequency for hemodialysis:
Most hemodialysis patients require 3-5hrs of dialysis 3days/week.
Limitations of dialysis:
Dialysis does NOT replicate the kidney’s synthetic functions –> EPO, vitD deficiency.
Complications associated with hemodialysis:
- Hypotension
- Relative hypo-osmolarity of the ECF compared with the brain may result in nausea, vomiting, headache, and rarely, seizures or coma.
- “1st use syndrome”.
- Complications with the anticoagulation.
- Infections of vascular sites –> sepsis.
Proteinuria - Definition:
Urinary excretion of >150mg protein /24h.
Asymptomatic TRANSIENT proteinuria:
Has an EXCELLENT prognosis - NO further evaluation is required.
Asymptomatic PERSISTENT proteinuria + Symptomatic proteinuria:
Require further work-up - high chance of renal disease in these patients.
Classification of proteinuria:
- Glomerular
- Tubular
- Overflow
- Other causes
Tubular proteinuria:
Small proteins normally filtered at the glomerulus then reabsorbed by the tubules appear in the urine because of abnormal tubules (ie due to decreased tubular reabsorption).
Proteinuria –> Tends to be less severe.
Tubular proteinuria - Etiology:
- SCA
- UT obstruction
- Interstitial nephritis
Overflow proteinuria?
Incr. production of small proteins overwhelms the tubules’ ability to reabsorb them - Bence-Jones in MM.
Other causes of proteinuria:
- UTI
- Fever, heavy exertion/stress, CHF.
- Pregnancy.
- Orthostatic proteinuria (!).
3 key features of nephrotic syndrome:
- Proteinuria
- Hypoalbuminemia
- Hyperlipidemia
Nephrotic syndrome - Patients are hyper or hypo-coagulable?
Hypercoagulable - due to loss of CERTAIN anticoagulants in the urine –> Incr. risk of thromboembolic events (DVT, Pulm. embolism, renal vein thrombosis).
Drugs that may cause nephrotic syndrome:
- Captopril
- Heroin
- Heavy metals
- NSAIDs
- Penicillamine
When is it possible for the urine dipstick to give false(-) results:
When predominant urinary protein is globulin - Light chains in myeloma.
Initial test when proteinuria is detected by dipstick test?
Urinalysis
Urinalysis - 3 main steps:
- Visual inspection of the urine - color, clarity.
- Dipstick reactions - pH, Protein, Glucose, blood, ketones, nitrite, Leukocyte esterase.
- Microscopic exam of the urine sediment - casts, cells, bacteria, WBCs, RBCs, crystals.
Persistent asymptomatic proteinuria - What to do first?
Start by checking BP and examining urine sediment –> Treat the underlying condition and associated problems (eg hyperlipidemia).
Symptomatic proteinuria - Treatment:
- Treat the underlying disease (DM, MM, SLE, minimal change disease).
- ACEIs.
- Diuretics - if edema.
- Limit dietary protein and sodium.
- Treat hyperCH - using diet or a lipid-lowering agent.
- Vaccinate against influenza and pneumococcus - there is an incr. risk of infection in these patients.
Hematuria - Definition:
> 3 erythrocytes/HPF on urinalysis.
Gross hematuria is commonly presenting sign in?
Patients with bladder cancer - 85%.
Patients with RCC - 40%.
Atraumatic hematuria - etiology?
Infections (cystitis, urethritis, prostatitis) –> 25%.
Stones 20%.
Drugs that can cause hematuria:
- Cyclophosphamide
- Anticoagulants
- Salicylates
- Sulfonamides
Infection cause gross or microscopic hematuria?
Either.
Test for hematuria?
Urine dipstick - sensitivity is >90%.
GN - Etiology:
- Generally caused by immune-mediated mechanisms.
2. Other mechanisms include metabolic and hemodynamic disturbances.
RPGN - What is it, basically?
A clinical syndrome that includes any type of GN in which rapid deterioration of renal function occurs over weeks to months, leading to renal failure and ESRD.
Possible presentations of glomerular disease:
- Isolated proteinuria
- Isolated hematuria
- Nephritic syndrome - hematuria, HTN, azotemia.
- Nephrotic syndrome - Proteinuria, edema, hypoalbuminemia, hyperlipidemia.
Minimal change disease - Associated with?
HL and NHLs.
Root cause of MCD:
Current evidence points to systemic T cell dysfunction as the most likely root cause of MCD.
FSGS accounts for 25% of cases of NEPHROTIC syndrome. Can hematuria and HTN be present?
Yes.
Prognosis of FSGS:
Fair to poor - Generally resistant to steroid therapy - patients develop renal insufficiency within 5-10yrs - Course is progressive.
FSGS Treatment:
- Remission is achieved in 50% of patients with the use of cytotoxic agents, steroids, and immunosuppressive agents.
- ACEIs/ARBs are also commonly indicated.
Etiology of membranous glomerulonephritis:
- Idiopathic
- 2o due to infection - Hep C, hep B, syphilis, malaria.
- Drugs - Captopril, gold, penicillamine.
- Neoplasm.
- Lupus.
MCC of GLOMERULAR HEMATURIA:
IgA nephropathy - Berger’s disease.
Gross hematuria is also common after what?
An URI or strenuous exercise.
IgA nephropathy - Electron microscopy:
Mesangial deposition of IgA and C3.
IgA nephropathy - Prognosis:
In most patients is good with preservation of renal function - renal insufficiency may develop in 25%.
IgA nephropathy - Treatment:
Some advocate steroids for unstable disease, but NO therapy has been proven to be effective.
Hereditary nephritis (Alport) - Inheritance pattern:
X-linked or AD with variable penetrance.
Hereditary nephritis - clinical presentation:
- Hematuria
- Pyuria
- Proteinuria
- High-frequency hearing loss without deafness
- Progressive renal failure
Hereditary nephritis - Treatment:
No effective treatment
Membranoproliferative GN is commonly associated with:
Cryoglobulinemia
Membranoproliferative GN - Prognosis:
Poor - RF in 50% - Treatment is rarely effective.
Rare serious complication of Post-strep GN:
RPGN - More commonly in adults.
Goodpasture - Lung or kidney comes first?
Lung disease precedes kidney disease by days to weeks. Associated with a variable course.
Goodpasture treatment:
- Plasmapheresis to remove circulating anti-IgG antibodies.
2. Cyclophosphamide and steroids can decrease the formation of new antibodies.
HIV nephropathy:
- Proteinuria, edema, hematuria.
2. Collapsing form of FSGS.
HIV nephropathy - Treat with:
- Prednisone
- ACEIs
- Antiretroviral therapy
Diagnosing acute interstitial nephritis (AIN):
- Look for a recent infection.
- Start of a new medication.
- Rash
- Fever
- General aches/pains
- Signs/Symptoms of AKI.
Acute interstitial nephritis (AIN) - General:
- Inflammation of the interstitium.
2. 10-15% of AKI.
AIN - Etiology:
- Acute allergic reaction to medication is the MCC.
- Infection, especially in children - due to a variety of agents, including strep and legionella.
- Collagen vascular diseases - Sarcoidosis.
- Autoimmune - SLE, Sjögren.
AIN - Clinical features:
- AKI and its associated features.
- Rash, fever, eosinophilia are the CLASSICAL symptoms.
- Pyuria and hematuria.
Diagnosis of AIN can be made if the patient:
Is known to have been exposed to one of the offending agents, and has the following:
- Rash
- Fever
- Acute renal insufficiency
- Eosinophilia
AIN - Diagnosis:
- Renal function tests - incr. BUN and Cr levels.
- Urinalysis - eosinophils.
- Mild proteinuria or microscopic hematuria may be present.
Is it possible to distinguish AIN from ATN based on clinical grounds alone?
It is often impossible –> Renal biopsy is required, but is usually NOT performed given its invasiveness.
AIN - Treatment:
- Remove the offending agent is usually enough to reverse the clinical findings.
- If Cr continues to increase after stopping the offending agent, steroids may help.
- Treat infection if present.
Acute vs Chronic AIN - Features of ACUTE:
Interstitial nephritis causes a rapid deterioration in renal function and is associated with interstitial eosinophils or lymphocytes.
Acute VS chronic AIN - Features of chronic:
Interstitial nephritis has a more indolent course and is associated with tubulointerstitial fibrosis + atrophy.
Renal papillary necrosis - Most commonly associated with:
- Analgesic nephropathy
- Diabetic nephropathy
- Sickle cell disease
- Urinary tract obstruction
- UTI
- Chronic alcoholism
- Renal transplant rejection
Renal papillary necrosis - Diagnosis:
Typically made by excretory urogram - Note change in papilla or medulla.
Renal papillary necrosis - Course:
The course is variable - Some patients have rapid progression, whereas others have a more indolent, chronic course.
Sloughed, necrotic papillae can cause:
Ureteral obstruction.
Analgesic nephropathy - Can manifest as:
- Interstitial nephritis
2. Renal papillary necrosis
Analgesic nephropathy may lead to:
- Acute RF
2. Chronic RF
Renal tubular acidosis - What is it?
A disorder of the renal tubules that leads to a non-anion gap hyperchloremic metabolic acidosis.
Glomerular function is normal.
Renal tubular acidosis - What characterizes it?
A decrease in the H excreted in the urine, leading to acidemia and urine alkalosis.
Renal tubular acidosis - How many types?
3 - Types 1, 2, 4.
RTA type 1 (distal):
Problem –> Inability to SECRETE H at the distal tubule –> New HCO3 cannot be generated –> Metabolic acidosis.
RTA type 1 - Effects:
Incr. exertions of ions (Na, Ca, K, Sulfate, Ph) with the following effects:
- Decr. in ECF volume.
- Hypokalemia
- Renal stones/Nephrocalcinosis –> Incr. Ca and Ph excretion into alkaline urine.
- Rickets/Osteomalacia
RTA type I leads to?
Hypokalemic, hyperchloremic, non anion gap met.acidosis.
RTA type 1 symptoms:
2o to nephrolithiasis and nephrocalcinosis - 70% have kidney stones.
RTA type 1 - Etiology:
- Congenital
- MM
- Nephrocalcinosis
- Nephrotoxicity - Amphoter B.
- Autoimmunes
- Medullary sponge kidney
- Analgesic nephropathy
RTA type 1 - Treatment:
- Correct acidosis with sodium HCO3 - Also prevents kidney stones, which is a major goal of therapy.
- Administer phosphate salts - promotes excretion of titratable acid.
RTA type 2:
Problem –> Inability to reabsorb HCO3 at the proximal tubule –> incr. excretion of HCO3 in the urine and metabolic acidosis.
Also, loss of K and Na in the urine.
RTA type 2 - Condition:
Hypokalemic, hyperchloremic non anion gap met. acidosis (as in RTA 1).
RTA type 2 - Etiology:
- Fanconi syndrome (child).
2. Cystinosis, Wilson, Lead, MM, Nephrotic syndrome, amyloidosis.
RTA type 2 - Why MM should always be ruled out in a patient with proximal RTA?
The excretion of monoclonal light chains is a common feature.
RTA type 2 - Do we see nephrolithiasis and nephrocalcinosis?
No, unlike RTA 1.
RTA type 2 - Treatment:
- Treat underlying cause.
- DO NOT give HCO3 to correct acidosis –> It will be excreted in the urine.
- Na restriction increases Na reabsorption (and thus bicarbonate reabsorption) in the proximal tubule.
RTA type 4:
Problem –> Any condition that is associated with hypoaldosteronism or incr. renal resistance to aldosterone.
RTA type 4 - Seen in:
Common in patients with:
- Interstitial renal disease
- Diabetic nephropathy
RTA type 4 - What happens?
Decr. Na absorption and decreased H and K secretion in the distal tubule.
RTA type 4 - Condition:
UNLIKE other types RTA, type 4 –> HYPERkalemia and acidic urine. A non anion gap metabolic acidosis still occurs.
RTA type 4 - Nephrolithiasis and nephrocalcinosis?
Rarely.
Hartnup syndrome - Inheritance pattern:
AR - Defective amino acid transporter.
Hartnup syndrome - Main problem:
Results in decr. intestinal + renal reabsorption of NEUTRAL amino acids, such as tryptophan, causing nicotinamide deficiency.
Hartnup syndrome - Clinical features:
Similar to pellagra:
- Dermatitis
- Diarrhea
- Ataxia
- Psychiatric disturbances
Hartnup syndrome - What to give?
Nicotinamide - If the patient is symptomatic.
Fanconi syndrome - What happens?
Hereditary or acquired PROXIMAL tubule dysfunction –> Defective transport of some of the following:
- Glucose
- Amino acids
- Na
- K
- Ph
- Urate
- HCO3
Fanconi syndrome - Associated with:
- Glycosuria
- Phosphaturia –> Skeletal problems.
- Proteinuria
- Polyuria
- Dehydration
- Type 2 RTA
- Hypercalciuria
- Hypokalemia
Fanconi syndrome - Treat with?
- Ph
- K
- Alkali and salt supplementation
- Adequate hydration
MCC genetic cause of CKD:
AD PKD –> ESRD develops in 50% of patients by late 50s or 60s.
Remainder have a normal life span.
–> Occurs from RECURRENT episodes of pyelonephritis/nephrolithiasis.
AD PKD presents with:
- Pain
- Hematuria
- Infection
- HTN
- Kidney stones
AD PKD - Associated findings:
- Intracerebral berry aneurysms (in 5%-20%) –> MOST do NOT rupture.
- Infection of cysts - Bleeding into cysts.
- Renal failure - late.
- Kidney stones.
- Heart valve abnormalities (especially MVP).
- Cysts in OTHER ORGANS (liver, spleen, pancreas, brain).
- Diverticula (colon).
- Hernias (abdominal/inguinal).
AD PKD - Treatment:
- No curative therapy is available.
- Drain cysts if symptomatic.
- Treat infections with antibiotics.
- Control HTN.
AR PKD - General features:
- Characterized by cysts predominantly in the renal collecting duct as well as hepatic fibrosis.
- Less common compared to AD PKD - True incidence is UNKNOWN since many affected newborns die without proper diagnosis.
- WIDE variety in the level of renal impairment. Most will eventually experience progressive RF.
AR PKD - Liver problems:
ALWAYS present - may be the dominant clinical feature especially in OLDER adults.
–> Portal HTN and cholangitis.
AR PKD - Pulmonary complications:
Pulmonary insufficiency 2o to pulmonary HYPOPLASIA + enlarged kidneys limiting diaphragmatic movement may be severe.
–> Leading cause of morbidity and mortality in the neonatal period.
Newborns with severe AR PKD may present with?
Potter syndrome, which is the constellation of clinical features associated with decr. amniotic fluid (oligohydramnios).
- Lung hypoplasia.
- Limb abnormalities.
- Characteristic abnormal facies.
AR PKD diagnosis:
- Detected prenatally due to widespread use of the US during pregnancy.
- Less severe cases may not be detected until much later.
- Molecular genetic testing may confirm the disease in cases where the diagnosis is unclear.
Medullary sponge kidney:
Cystic dilation of the collecting ducts.
- Hematuria
- UTI
- Nephrolithiasis
- Asymptomatic
Medullary sponge kidney - Thought to be associated with:
- Hyperparathyroidism
2. Parathyroid adenoma
Simple renal cysts:
Very common - 50% of people >50. Incidence incr. with age.
Renal artery stenosis - Etiology:
- Atherosclerosis - 66% of cases.
- Bilateral in 1/3 of cass.
- Smoking + CH are predisposing factors. - Fibromuscular dysplasia - Usually in young females, Bilateral in 50% of patients.
Renal artery stenosis - Abdominal bruits:
RUQ, LUQ, or epigastrium –> Present in 50-80%(!) of patients.
Especially in those with fibromuscular hyperplasia.
Renal artery stenosis - Diagnosis:
Gold standard –> Renal arteriogram, but contrast dye can be nephrotoxic - do NOT use it in patients with renal failure.
ACEIs in patients with renovascular HTN:
Should be used carefully.
Renal artery stenosis - How to diagnose in patients with renal failure?
MRA is a new test - Magnetic dye is NOT nephrotoxic, so it can be used in patients with renal failure.
Suspect renovascular HTN in the following situations:
- Malignant HTN
- Sudden onset of HTN
- HTN that suddenly worsens
- HTN refractory to standard therapy
Renal artery stenosis - Treatment:
- Revascularization with percutaneous transluminal renal angioplasty (PRTA) –> Initial treatment in most patients.
- Surgery if PRTA is NOT successful (bypass).
- Conservative therapy (ACEIs, CCBs).
Renal vein thrombosis - Seen when?
- Nephrotic syndrome
- RCC
- Trauma
- Pregnancy/OCPs
- Extrinsic compression (retroperitoneal fibrosis, aortic aneurysm, lymphadenopathy).
- Severe dehydration –> Infants.
Renal vein thrombosis - Diagnosis:
- Selective renal venography (definitive study)
2. IVP
Atheroembolic disease of the renal arteries:
Showers of cholesterol crystals that dislodge from plaques in large arteries and embolize to the renal vasculature.
Hypertensive nephrosclerosis - Definition:
Systemic HTN increases capillary hydrostatic pressure in the glomeruli, leading to benign or malignant sclerosis.
2nd MCC of ESRD:
HTN –> Nephrosclerosis
Benign nephrosclerosis - What happens:
- Thickening of the glomerular afferent arterioles develops in patients with long-standing HTN.
- Results in mild to moderate incr. in Cr levels, microscopic hematuria, mild proteinuria.
- Advanced disease –> ESRD.
Malignant nephrosclerosis - What happens?
Rapid decr. in renal function and accelerated HTN due to diffuse intrarenal vascular injury.
Malignant nephrosclerosis - Clinical manifestations:
- Markedly elevated BP.
- Rapid incr. in Cr, proteinuria, hematuria, RBC and WBC casts in the urine sediment, and sometimes nephrotic syndrome.
- Microangiopathic hemolytic anemia may also be present.
HTN nephrosclerosis - Treatment:
Control BP - In both benign/malignant nephrosclerosis.
Not clear which agents should be used in the chronic setting, or how effective they are once frank albuminuria is present.
Nephrolithiasis - Sites of obstruction:
- Ureterovesicular junction - MC site of impaction.
- Calyx of the kidney.
- Ureteropelvic junction.
- Intersection of the ureter and the iliac vessels (near the pelvic brim).
MC risk factor for nephrolithiasis:
Low fluid intake.
Nephrolithiasis - Males or females?
Males 3x more common.
Causes of hypercalciuria:
- Incr. intestinal absorption of Ca.
- Decr. renal reabsorption of Ca.
- Incr. bone reabsorption of Ca.
- Primary hyperparathyroidism.
- Sarcoidosis.
- Malignancy.
- VitD excess.
Causes of hyperoxaluria:
- Severe steatorrhea of any cause can lead to Ca oxalate stones - due to absorption of oxalate.
- Small bowel disease.
- Crohn.
- Pyridoxine deficiency.
Struvite stones (staghorn stones) - Organisms:
- Proteus
- Serratia
- Klebsiella
- Enterobacter
Hexagon shaped crystals?
Cystine stones.
Nephrolithiasis - Clinical course:
- If a stone is >1cm, it is unlikely to pass spontaneously.
- Stones <0.5cm usually do pass spontaneously.
- Recurrence is common. Up to 50% of the patients have recurrences within 10yrs of having the first stone.
Classic presentation of nephrolithiasis:
- Sudden onset of colicky flank pain that radiates into groin.
- Urinalysis showing hematuria.
Nephrolithiasis - Clinical features:
- Renal colic.
- Nausea and vomiting are common.
- Hematuria (in over 90% of the cases).
- UTI
Hematuria + Pyuria indicates?
A stone with concomitant infection.
Having the stone for analysis is helpful?
Yes - Both in treatment and in preventing recurrence. Patient should attempt to recover the stone that is passed (strain urine).
Nephrolithiasis - Gold standard for diagnosis:
CT scan (spiral CT) WITHOUT CONTRAST.
Urinary tract obstruction - Evaluation:
- Duration of symptoms.
- UTI
- History of nephrolithiasis.
- History of surgery.
- Suprapubic mass (distended bladder)
- Flank mass (hydronephrosis)
- Features of CKD
UT obstruction - Clinical features:
- Renal colic and pain - More common with acute obstruction. May manifest only DURING urination.
- Oliguria.
- Recurrent UTIs.
- Hematuria/Proteinuria.
- Renal failure.
What should be done if the patient has acute UT obstruction + a UTI?
Emergent diagnostic tests are indicated –> Renal US or excretory urogram.
–> Intervene immediately to relieve obstruction.
Prostate cancer - Risk factors:
- Age - Most important.
- African-American race.
- High-fat diet.
- Positive family history.
- Exposure to herbicides and pesticides.
PSA-DRE-TRUS (transrectal US) - If PSA>10?
TRUS with biopsy is indicated - regardless of DRE findings.
PSA-DRE-TRUS - If DRE is abnormal?
TRUS with biopsy is indicated, regardless of PSA level.
PSA-DRE-TRUS - If PSA<4 + DRE is negative?
Annual follow-up is indicated.
PSA-DRE-TRUS - If PSA is 4.1-10 and DRE is negative?
Biopsy is usually recommended.
Normal prostate feels like a?
Thenar eminence.
What does it mean when a hard, nodular knuckle in the prostate is palpable?
60-70% have spread beyond the prostate.
DRE changes PSA levels?
NO - Prostatic massage does.
The combination of PSA and DRE can detect up to ?
60% of prostate cancers while they are still localized.
Key points about the PSA:
- The higher the PSA, the higher the cancer risk.
- Normal PSA does not rule out prostate cancer.
- Not used as a screening test.
- If a patient requests the test, order it.
TRUS with biopsy - Indications:
- PSA>10 (chance of finding cancer is over 50%).
- PSA velocity >0.75 per yr.
- Abnormal DRE.
Stages of prostate cancer:
Stage A –> Nonpalpable, confined to prostate.
Stage B –> Palpable nodule, but confined to prostate.
Stage C –> Extends beyond capsule without metastasis.
Stage D –> Metastatic disease.
MC complications of prostatectomy:
- Urinary incontinence
2. Erectile dysfunction
RCC - More common in men or women?
MEN 2:1.
RCC - Familial type?
Less than 2% occur as part of AD VHL syndrome.
RCC - Areas of metastasis:
- Lung
- Liver
- Brain
- Bone
How many RCC are discovered incidentally on a CT scan or US performed for other reasons?
Up to 20-30%.
RCC - Risk factors:
- Smoking
- Phenacetin analgesics (high use)
- AD PKD
- Chronic dialysis - Multicystic disease develops.
- Exposure to heavy metals (mercury, cadmium).
- HTN.
RCC - Clinical features:
- Hematuria MC symptoms - 70%.
- Abdominal or flank pain - 50%.
- Abdominal mass - 40%.
- Weight loss, fever.
- Paraneoplastic syndromes (uncommon).
RCC - Diagnosis:
- Renal US - For detection of renal mass.
- Abdominal CT with AND without contrast - optimal test for diagnosis and staging - perform if US shows a mass or cysts.
RCC Treatment:
Radical nephrectomy - excision of kidney + adrenal + Gerota fascia with excision of nodal tissue along the renal hilum –> For stages I to IV.
MC type of tumor of the GUT:
Bladder carcinoma - 90% are transitional cell carcinomas, 5% SCC, 2% ADENOCA.
Bladder cancer - MC route of spread?
Local extension to surrounding tissues.
Likely to recur after removal.
Bladder cancer - Risk factors:
- Smoking
- Industrial carcinogens (aniline dye, azo dyes).
- Long-term treatment with cyclophosphamide –> May cause hemorrhagic cystitis –> incr. risk for TCC.
Bladder cancer - Clinical features:
- Initial presenting sign is HEMATURIA in most cases - painless hematuria is the classic presentation.
- Irritable bladder symptoms, such as dysuria frequency.
Bladder cancer - Diagnosis:
- Urinalysis and urine culture - To rule out.
- Urine cytology - To determine malignant cells.
- IVP
- Cystoscopy and biopsy (definitive test).
- Chest radiograph and CT scan - for staging.
Testicular cancer - Risk factor:
- Cryptorchidism - Surgical correction does NOT eliminate the risk.
- Klinefelter’s syndrome.
Testicular cancer - Clinical features:
- Painless mass/lump/firmness of the testicle - because of lack of pain, may go unnoticed by the patient until advanced.
- Gynecomastia may be present because some of the non seminomatous germ cell tumors produce gonadotropins.
Testicular cancer - Diagnosis:
- Physical exam - testicular mass.
- Testicular US - initial test for localizing the tumor.
- Tumor markers - helpful in diagnosis, staging, and monitoring response to therapy.
- CT scan and chest radiograph for staging.
Tumor markers in testicular cancer:
- β-hCG –> Always elevated in choriocarcinoma - May be elevated in non seminomatous germ cell tumors as well.
- AFP –> Incr. in embryonal tumors (in 80% of the cases) - Choriocarcinoma and seminoma never have an elevated AFP.
DDX of testicular cancer:
- Varicocele
- Testicular torsion
- Spermatocele
- Hydrocele
- Epididymitis
- Lymphoma
Staging of testicular cancer:
Boden-Gibb:
Stage A –> Confined to testis/cord.
Stage B –> Retroperitoneal lymph node spread (below diaphragm).
Stage C –> Distant metastasis.
Penile cancer - Peak incidence:
60-70
Penile cancer - Associated with:
- HSV
2. HPV 18
Testicular torsion - Timeframe:
If surgery is delayed beyond 6hrs, infarction may occur, and the testicle may not be salvageable.
Epididymitis - Target:
Childer/elderly –> E.coli.
Young men –> Gonorrhea, Chlamydia.
Epididymitis - Clinical features:
- Swollen, tender testicle.
- Dysuria
- Fever/chills
- Scrotal pain
- Scrotal mass
Epididymitis - May be difficult to DDX from:
Torsion –> Not associated with fever + acute onset.
Definition of AKI (acute kidney injury):
Rapid decline in renal function, with an increase in serum creatinine level (a relative increase of 50% or an absolute increase of 0.5-1.0 mg/dL).
Creatinine may be normal despite a markedly reduced GFR in the early stages of AKI due to the time it takes for creatinine to accumulate in the body.
