Formula for Osmolal gap
Calculated Osm = 2 (Na) + BUN/2.8 + Glucose/18
Osm gap = Measured - Calculated
Normal OG < 10
Briefyly discuss Isopropyl alcohol ingestion
What is it metabolized to?
What acid-base characteristic does it have?
Metabolized to acetone. Causes Osmolar Gap and Ketosis, but no AG
Briefly discuss Ethylene glycol ingestion
How is it ingested as?
What is its acid-base feature?
What can it cause?
What is the treatment?
Ingested as antifreezeCan cause profound shockAnion gap metabolic acidosis, osmolar gapMetabolized to calcium oxalate crystals in urineTreatment: fomepizole, folic acid, dialysis
Briefly discuss Propylene Glycol:
Where is it found?
What can it cause?
Solvent in IV lorazepam, diazepam, and propofol which can cause lactic acidosis
What are the mechanisms of Non-AG Metabolic Acidosis?
Loss of HCO3: Diarrhea, Ureteroenterostomy (ileal loops)Inability to excrete H+: RTAExogenous Acid: TPN -- Addition of lysine, arginine
Discuss Non-Anion Gap Metabolic Acidosis:
When is it seen?
How do you differentiate from its causes?
Seen in Diarrhea and RTADifferentiate the two above by measuring Urine AGUAG = (UNa + UK) - UClServes as a measure of kidney's ability to generate ammoniumIn non-AG acidosis, calculate UAG: Negative UAG = Diarrhea: kidney generates NH4, urine Cl increases Positive UAG = RTA: NH4 production is impaired
What are the Distal RTAs?
Type 4 or Type 1
What RTA is proximal?
Which RTAs are hypokalemic?
Type 1 and 2
Which RTA is hyperkalemic
Discuss Distal, Type 1 RTA:
What is the defect?
What is the urine pH?
What are its associations?
Can't excrete H+ ions across concentration gradientUrine pH never less than 5.5, despite presence of acidemiaAssociated with hypercalcemia, stones, nephrocalcinosisEtiologies: Amphotericin, toluene, hypergammaglobulinemiaTreatment: Potassium and HCO3 replacement, Shohl's solution
What are possible etiologies of Distal Type I RTA?
What is the treatment for Distal Type I RTA?
K and HCO3 replacement
What disorders are associated with Distal Type I RTA?
Discuss Proximal, Type II RTA:
What is the urine pH?
Mechanism: Bicarb wastingUrine pH is high early in course, then falls as serum pH fallsEtiologies: Drugs - CA inhibitors, amphotericin, heavy metals, myeloma, Sjogren's syndromeLook for Fanconi Syndrome: hypophos, hypouricemia, glycosuria, AAuria (coal -- cysteine, ornithine, arginine, lysine)Treatment: lots of HCO3
What are the etiologies of Proximal Type II RTA?
Carbonic Anhydrase inhibitorsAmphotericinHeavy metals MyelomaSjogren's syndrome
Discuss Distal, Type 4 RTA:
Hyperkalemic, hyperchloremic metabolic acidosisMechanism: usually hyporenin, hypoaldoEtiology: - DM, most common - Obstructive uropathy - Interstitial renal disease, sickle cell disease - Drugs: cyclosporineTreatment: HCO3, furosemide, Florinef
Metabolic alkalosis that is Chloride sensitive (UCl < 10) is caused by?
Vomiting: UGI lossesDiureticsPost-hypercapniaCF
Metabolic alkalosis with UCl > 10 (Chloride Resistant) without HTN is likely caused by?
Bartter syndromeGitelman syndromeSurrptitious diuretics
Metabolic alkalosis that is chloride resistant (UCl > 10) with HTN is likely caused by?
Exogenous steroidsEndogenous steroids10 hyperaldoCushing's 11-OH deficLiddle syndrome
Discuss Bartter Syndrome:
What is the renin and ado level?
What is the calcium level?
Where is the defect?
What is the treatment?
HypokalemiaMetabolic alkalosis and normal BPLow mag, high renin and aldoHypercalciuria No chondrocalcinosisDefect in the Ascending LoopLooks like the pt is taking a loop diureticRx: NSAIDs, K
Discuss Gitelman syndrome
Is the BP high or low?
What is the calcium level
What is it associated with?
Where is the defect?
The pt looks like he is taking what medication?
What is the treatment?
Metabolic alkalosis and normal BPLow K, low MgHypocalciuriaAssociated with ChrondrocalcinosisDefect in the Distal Convoluted TubuleLooks like the pt is taking a thiazide diureticTx: Magnesium, K, sometimes amiloride or spironolactone
What is the best intervention in Hypotonic hyponatremia associated with Edema states (CHF, cirrhosis, nephrotic syndrome) and RF? (High ECF Volume)
What urine and serum studies are you going to look for and how will they look?
What do you always rule out?
What is the treatment?
UOsm inappropriately high for low SOsm, low uric acid levelsAlways R/O Addison diseaseRx: Demeclocycline, Lithium, Vasopressin receptor antagonists (cornivaptan)
Etiologies of Nephrogenic Diabetes Insipidus:
Hereditary: X-linked defect in V2 receptot geneDrugs: Lithium, Demeclocycline, AmphotericinElectrolytes: Hypercalcemia, hypokalemiaSjogren's
Treatment for Nephrogenic Insipidus?
What is the treatment for Nephrogenic DI caused by Lithium toxicity?
What are the ECG changes of hyperkalemia?
Peaked T wavesWidened QRSLoss of P wavesBradyarrhythmias
Causes of Hypocalcemia:
CKDHypoparathyroidismPseudohypoparathyroidismHypomagAcute PancreatitisRhabdomyolysisVitamin D Deficiency
What are causes of Hypercalcemia?
1. Endo causes: - High PTH - Hyperthyroidism - Addison's2. Granulomatous Dis -- Sarcoid, TB3. Malignancy4. Toxicity -- Vitamin A or D, Thiazides, Milk-Alkali syndrome5. Familial Hypocalciuric Hypercalcemia
What drugs cause Hypomagnesemia?
"The Amish Pay Cash for their Penthouse"
Etiologies of Hypophosphatemia
Alcoholic KetoacidosisDKARefeeding/HyperalPhosphate bindersHyperPTH
Complications of Hypophosphatemia:
Hemolysis, Thrombocytopenia, Poor WBC functionRhabdoMuscle paralysis
Discuss effect and use of Carbonic Anhydrase Inhibitors
Where does it work?
What can it cause?
What is it used for?
Works in the proximal tubuleCauses a Type II RTACauses a metabolic acidosis, so used for treatment of met. alkalosis, mountain sickness, glaucoma
Discuss effect and uses of Loop diuretics:
Inhibit Na-K:2Cl channelUseful in hypercalcemia, Type 4 RTA
Range of Pre-HTN BP?
Stage I HTN ?
Stage 2 HTN
?160 / ?100
Discuss Primary Hyperaldosteronism:
Discuss hypertension secondary to 11-OH deficiency:
There is high cortisol, low renin and low aldosterone.Glycyrrhizic acid also inhibits 11-hydroxysteroid dehydrogenase
What is Liddle syndrome?
What pertinent labs point toward this diagnosis?
What is the treatment?
HTN with low K and metabolic alkalosisAbnormality is in salt absorptionDefect in the amiloride sensitive Na channel results in chronic volume expansionLow renin, Low aldo levelsAutosomal dominantTreatment: triamterene and Na restriction
What is the normal Protein level in a 24-hour urinc collection?
How about in a normal "spot" urine protein/creatinine ration?
<150 mg/day< 200 mg/g (.2) in a spot urine
What are the causes of sterile pyuria?
TBprostatitisanalgesic abuse nephropathy
In a pt with hematuria, what would make you suspect an upper tract source?
RBC castsProteinuriaElevated creatinine
What are the diseases associated with the ff casts?
1. RBC casts
2. WBC casts
3. RTC casts
4. Granular ("dirty brown") casts
5. Waxy casts
1. Glomerulonephritis2. Pyelo3. Interstitial inflammation4. ATN5. CKD
Discuss Diagnostic studies for ARF
UAFENU/S of kidneyRenal bx if ARF unresolved or unexplained
Discuss Acute Interstitial Nephritis
Always consider when ARF occurs with patient on a new medicationClinical clues: rash, fever, eosinophiliaUA: renal tubular cells +/- castsEosinophils in the urine (Wright or Hansel stain)
Drugs that can cause Acute Interstitial Nephritis
NSAIDsAntibiotics: PCN, sulfa, cephalosporins, rifampin, quinolones
Discuss AIN (Acute Interstitial Nephritis) secondary to NSAIDs
May occur months after beginning NSAID in patients with normal renal fxnAIN with nephrotic range proteinuriaThis is different than the pre-renal ARF that NSAIDs cause in patients with pre-existing renal disease
ARF with FEN > 2% point toward what diagnosis?
What casts is assoc with this?
ATNMuddy brown cast
What type patient is at risk for Radiocontrast Nephropathy?
Interventions to reduce risk of Radiocontrast Nephropathy?
.9 NS 1 ml/kg/kg for 24 hourLow osmolality contrast, lowest dosePrevention: N-acetylcysteine, NaHCO3Stop metformin, diuretics, NSAIDs
*Please note that this is an exception -- FENa may be low
Who is at risk for Gadolinium Contrast induced Nephrogenic Systemic Fibrosis?
ARF or CKD with GFR < 30 ml/minARF due to hepatorenal syndrome or post-op liver transplant
What is Nephrogenic Systemic Fibrosis?
Tightening of the skin of trunk and extremities, unlike scleroderma, spares face.May affect internal organs
Discuss Minimal Change Disease
Presentation: Sudden onset, severe nephrtoic syndromeMost common in children, but 10-15% of adult cases of NSUsually GFR is normal, no HTNMost cases are idiopathicMay be caused by NSAIDs, also assoc with Hodgkin DiseaseTreatment: steroids, especially in children, may need cytotoxics in adults
What is the only pathologic finding in Minimal Change Disease?
Foot process fusion along the GBM seen on EM
Most common cause of idiopathic nephrotic syndrome in African-AmericansFrequently associated with reduced GFR, HTN and progressive renal failureMost common etiology is idiopathic - HIV-associated Nephropathy - Reflux nephropathy - ObesityTx: ACE-I, ARB, steroids
What would you suspect in an elderly pt with severe nephrotic syndrome?
Suspect Primary (AL) AmyloidosisUsually rapidly progress to end-stage diseaseAssociated with overproduction of light chainsAssoc with other organ involvement, i.e., hepatomegaly, restrictive CMPDiagnosis: SPEP, UIEP, BiopsyResponds poorly to treatment
What other differential diagnosis would you have on a pt with nephrotic syndrome with long-standing inflammation, i.e., Familial Mediterranean Fever, TB, RA?
Secondary AmyloidosisIn FMF, colchicine prevents amyloidosisAlways consider MM as etiolgyRate of progression slowed with eprodisate
In Familial Mediterranean Fever, what medication can prevent amyloidosis?
What can slow the rate of progression of nephrotic syndrome in a pt with Secondary Amyloidosis?
Which Nephritic syndrome has low complement?
10 Post-infectious GN MPGN
20 SLE Endocarditis Cryoglobulinemia
Which Nephritic Syndrome has normal complement?
10ANCA (+) RPGNIgA NephropathyAlport syndrome
Briefly describe the presentation of a pt with Nephritic Syndrome
ProteinuriaHematuria� RBC castsReduced GFRSalt and water retention
Briefly discuss Post-infectious Glormerulonephritis
Post-infectious GN: occurs after many types of infections. Classic is post-strep Latent period: PSGN occurs 7-10 days after URI and up to 30 days after skin infection Requires nephritogenic strain of strepMost commonly presents with gross hematuraLabs: ASO positive C3 falls and returns to normal after 6-8 weeksGenerally self-limited
What are characteristic pathology features in the renal bx of a pt with Post-infectious GN?
Subepithelial humps on EM, which are immune complexes
What are the clinical features of Lupus Nephritis?
Proteinuria -- 100%Nephrotic syndrome -- 45 - 65%RBC casts -- 10%Microscopic hematuria -- 80%Decreased GFR -- 40-80%
WHO Classification for Lupus Nephritis
I Normal GlomeruliII MesangialIII Focal proliferativeIV Diffuse proliferativeV Membranous
What is the treatment of Lupus Nephritis with proliferative lesions?
Steroids with cyclophosphamide or MMF
What is the treatment for lupus nephritis with Mesangial (class II) classification?
What about Proliferative (class II or IV)?
Steroids for Mesangial lupus nephritisPulse steroids and cyclophosphamide, or later MMF, or just MMF and steroids for Proliferative lupus nephritis
Briefly discuss Mixed Essential Cryoglobulinemia
Typically associated with HCVClinical presentation: purpuric skin lesions, polyarthralgias, glomerulonephritisLabs: C4 low, RF +, "mixed" IgG-IgM cryoglobulins+25% will be mixed "nephritic" and "nephrotic"Renal disease may improve with treatment of HCV, relapses common
What is the usual clinical presentation in Mixed Essential Cryogobulinemia
purpuric skin lesionspolyarthralgiasglomerulonephritis
What lab result would you expect to see in a pt with Mixed Essential Cryoglobulinemia
C4 lowRF +"mixed" IgG-IgM cryoglobulins+25% will be mixed "nephritic" and "nephrotic"
What are the three types of Rapidly Progressive GN (RPGN)?
Histologic hallmark is the "crescent"
1. ANCA (+) = Pauci-immune GN (No immune deposits)2. Anti-GBM Antibody disease - Goodpasture Syndrome - Idiopathic Anti-GBM Ab GN3. Immune Complex-Mediated RPGN - SLE, Post-infectious GN (some cases only) - IgA Nephropathy
Briefly discuss ANCA (+) RPGN (Pauci-immune RPGN):
What needs to be urgently done?
Presents as insidious, rapidly progressive GN with HTNRepresents a "microscopic" polyangiitisSerology (-) except ANCARequires urgent renal bx: Only finding is extracapillary proliferation -- "crescents"Treatment: "pulse" methylprednisolone, cyclophosphamide
What typically presents with gross hematuria immediately after URI? (no latent period like PSGN)
Briefly discuss IgA Nephropathy
Very common form of GN world-wideTypically presents with gross hematuria immediately after URIPts frequently have normal GU eval before referral for renal biopsyRare in Af-AmProgressive renal failure in some patients, especially if severe proteinuria and/or hypertension
How do you confirm the diagnosis of IgA Nephropathy?
What renal disease is associated with nerve deafness?
Hereditary nephritis: Alport SyndromeFamilial renal disease, usually X-linkedPatients typically present with hematuria immediately following URI (lack of latent period distinguishes from Post-Strep GN)Ocular disorders may be associatedPrimary abnormality is defect in alpha-5 subunit of Type IV collagen
How do patients with Hereditary Nephritis typically present?
Patients typically present with hematuria immediately following URI (lack of latent period distinguishes from Post-Strep GN)May come with nerve deafness, usually men (X-linked familial renal disease)May also have ocular disorders
Briefly discuss Goodpasture Syndrome
Anti-GBM antibodies, acute GN, pulmonary involvementUsually present with hemoptysis, dyspneaTreatment: Plasmapheresis, high-dose steroids
What is you differential diagnosis for a patient who present with hemoptysis and dyspnea?
Goodpasture SyndromeWegener granulomatosisLupus and other vasculitidesInfcetious endocarditis (right sided)Sarcoidosis
What is a characteristic pathology of Goodpasture Syndrome?
Briefly discuss PAN
Affects medium-sized arteries, multi-system involvementRenal involvement due to renal aneurysms leading to renal ischemia/infarction
How do you diagnose PAN?
What is the treatment for PAN?
"pulse" steroidscytotoxic drugs
Briefly discuss Wegener Granulomatosis:
Present most commonly with renal disease associated with involvement of upper and lower respiratory tract.Treatement: "pulse" steroids and cytotoxic drugs
High dose steroids not effective with nephrities, so this is combined with cyclophosphamide and plasmapheresis
How is Wegener's Granulomatosis diagnosed?
granulomas on biopsyvasculitisC-ANCA (+)
In a pt with HUS or TTP, what would you expect to see on the renal biopsy?
What are the essential labs needed in the initial workup of the Nephritic Syndrome?
Complement levelsANAHepatitis studiesANCA Blood CxLupus studiesASO titersAnti-GBM antibodiesAnd finally, Renal biopsy
What is the standard initial treatment for Goodpasture's Syndrome?
What is the classic presentation of a pt with Analgesic Abuse Nephropathy?
Chronic interstitial nephritis with little proteinuriaMay present with acute flank pain due to papillary necrosisWill have sterile pyuriaImaging shows papillary necrosisCan be contributed to by Tylenol
What else can cause papillary necrosis?
sickle cell diseaseDM with pyelo
When do you screen for berry aneurysms in patients with Polycystic Kidney Disease?
Not done routinelyIt is recommended for those with PCKD with symptoms suspicious for aneurysm and those with family history of PCKD and aneurysms
Once a renal patient's GFR decreases to < 60 ml/min, what is your next intervention?
Monitor for Renal OsteodystrophyScreen for secondary hyperparathyroidismMonitor calcium and phosphorusMeasure iPTHAlk phos may be elevatedGoal is to keep Ca X Pho < 55
For pts at risk for renal osteodystrophy, what is the amount of Phosphorus you would recommend in their diet?
750 - 1000 mg/day
What interventions would you order to control phosphorus in a patient with renal osteodystrophy?
Dietary restriction of phosphorus (750-1000 mg/day)Ca-containing phosphate binders: Calcium CO3 or Calcium acetateSevelamer or lanthanumAl (OH)3
What intervention would you order for a pt with Renal Osteodystrophy and elevated PTH?
Measure serum 25-OH Vitamin D level1, 25 Vit D3 (calcitriol) or Vit D analogues (zemplar, Hectorol)Calcimimetic agent - Cinacalcet
What is the appropriate intervention for CRF patients with metastatic calcifications and uncontolled hyperparathyroidism?
Briefly discuss Anemia management in a pt with Stges 3,4,5 CKD:
Goal Hgb is 11-12If Hgb is < 11, check for iron deficiency with Fe TIBC, Sat and FerritinTarget ferritin value is >100Target Iron saturation >20%If Hgb < 11, give erythropoietin
In patients with CKD, explain why you have to treat acid excess
It may exacerbate anorexia and bone disease.Keep serum HCO3 > 20
What are the absolute indications for dialysis in patients with GFR < 15 mL/min?
What is the diagnostic criteria for CAPD peritonitis?
PD fluid WBC count > 100 with > 50% PMNs
Recommended empiric therapy for CAPD peritonitis?
IP Vancomycin or cefazolin and ceftazidime/cefepime (or gentamicin)
In patients with kidney transplant, what is the usual immunosuppression regimen?
Triple therapyPrednisonCyclosporine or tacrolimus and/or sirolimusCelcept
What is the usual infection prophylaxis in pts with kidney transplant?
What drugs can raise the levels of cyclosporine and tacrolimus?
What drugs can lower the levels of cyclosporine and tacrolimus?
What is the treatment of acute rejection in patients with renal transplant?
high dose steroidsPolyclonal or monoclonal antibodies
What are the physiologic changes of the kidney in pregnancy?
Kidneys enlargeSalt and water retention occur Serum Na falls, BUN falls Respiratory alkalosis Uric acid falls, can have renal glycosuriaSVR falls: BP falls, normal always < 120/80GFR rises: normal Scr < 0.8 mg/dL
HTN and proteinuria beginning after the 20th week of pregnancyEdema no longer part of the definitionIf these sx occur in early pregnancy, suspect underlying chronic renal disease
Define Severe Preeclampsia with HELLP Syndrome
Hemolysis - abnormal peripheral smear - bilirubin > 1.2 - LDH > 600Elevated LFT - AST > 70Low Platelets: < 100,000
What is the clinical presentation of the Acute Fatty Liver of Pregnancy?
Primigravida (> 50%)feverabdominal painnausea and vomitingafter 35th week
What is the exam and lab result in Acute Fatty Liver of Pregnancy?
Exam: jaundice, HTN, edema, abdominal painLab: hyperbiliruvinemia, mild elevation of transminases, hepatic/renal failure
What is the treatment of Acute Fatty Liver of Pregnancy?
termination of pregnancy
What is the diagnosis in a Post-partum pt with acute renal failure, anemia, HTN?
Idiopathic Post-Partum Renal FailureClinical Features: - Microangiopathic hemolytic anemia- Renal thrombotic microangiopathy- Acute renal failure- Malignant HTN- ThrombocytopeniaBegins days to weeks following a normal pregnancyTreatment: usually plasma exchange, ? steroids
Calcium Stone Treatment
All patients- increase water intake, reduce protein- increase diet vegetables and fruit- Reduce dietary NaClHyercalciuria -- treat with HCTZHypocitraturia -- treat with K-citrateHyperocaluria -- diet, pyridoxineHyperuricosuria -- allopurinol
Uric Acid Stone Treatment
Hyperuricosuria?- reduce dietary purines- allopurinolPersitently acid urine- KHCO3, K citrate, NaHCO3 to keep urine pH > 6.5 - 7- Reduce dietary proteinChronnic volume depletion: chronic diarrhea- correct it
What are "Coffin-lid" crystals?
Triple phosphate crystals that have coffin lid appearanceUsually due to recurrent UTI caused by urease splitters, i.e., proteus, providencia, klebsiellaUrolotic removal of stoneAppropriate antibiotics
What are interventions to treat and prevent Cysteine stones?
Keep urine output > 2.5 - 3 L/dayKHCO3 to keep urine pH > 7 - 7.5Treatment: D-penicillamine or tiopronin -- forms more soluble mixed disulfides with cysteine that are more soluble than cysteine
Describe Cystine stones
OctagonalLook like "Stop signs."
What are the characteristics of Immune complex-mediated glomerular nephritis?
HypocomplementemiaDysmorphic erythrocytesErythrocyte casts seen on urinalysis
Associated with HIV infection, syphilis, Hep C, or any chronic infection
Muddy brown casts on urinalysis point toward what kind of pathology?
What is pigment nephropathy?
It is a form of AKI that results after muscle injury leads to the release of myoglobin and other intracellular muscle contents into the circulation. Myoglobin is known to cause nephrotoxicity by induction of kidney ischemia and tubular obstruction that results in a form of AKI known as pigment nephropathy.
When should you consider a diagnosis of rhabdomyolysis?
A diagnosis of rhabdomyolysis should be considered in patients with a serum creatine kinase level above 5000 U/L (83.5 �kat/L) who demonstrate heme positivity on urine dipstick testing in the absence of hematuria
What are complications of rhabdomyolysis?
HypocalcemiaHyperphosphatemiaHyperuricemiaMetabolic acidosisAtue muscle compartment syndromeLimb ischemia
How do you manage a pt with ADPKD who present with BP 140/90?
BP target in pts with ADPKD is less than 125/75Frontline med is ACE-I or ARB
What intervention would you recommend on a pt with ADPKD who present with low-grade fever and gross hematuria?
Rule out infection which usually present with flank pain and bland urine. Low-grade fever and flank pain are the usual presentation in patients with cyst hemorrhage.These episodes are most often self-limited and bed rest and increased fluid intake shorten the duratio of gross hematuria.
In a pt with ADPKD, what is associated with low risk for disease progression?
Small kidney sizeAbsence of HTN or proteinuria
What is the gold standard for diagnosis renovascular hypertension due to fibromuscular dysplasia?
intra-arterial digital subtraction angiography
In a pt with Stage IV CKD and anemia, what level of ferritin and transferrin saturation is diagnostic of iron deficiency?
A transferrin saturation below 20% and a serum ferritin level below 100 ng/mL (100 �g/L) are diagnostic of iron deficiency in predialysis patients with CKD.
What is the treatment for patients with myeloma kidney?
Chemo and plasmapheresisDialysis also if with symptomatic uremia
What is the initial management of a pt with myeloma cast nephropathy?
volume expansionalkalinization of the urinediscontinuation of nephrotoxic agentsavoidance of radiocontrast agents
What is Tumor Lysis Syndrome?
It is caused by urate deposition and calcium phosphate ppt within the renal tubulesDevelop after initiation of chemo and can occur spontaneously in pts with a hign tumor burdenCan manifest as acute oliguric kidney injury accompanied by increased serum uric acid, phos, and potassium levels
What patients are at high risk for Tumor Lysis Syndrome, and what is the recommended treatment?
High risks are: 1. Burkitt lymphoma2. NHL lymphoblastic3. Burkitt acute lymphoblastic leukemia4. ALL with leukocyte count ?100,000/uL5. AML with leukocyte count ?50,000/uL6. serum uric acid levels higher than 7.5 mg/dL (0.4 mmol/L)
Treatment: Hydration + Allopurinol + rasburicase
What patients are at Intermediate risk for Tumor Lysis Syndrome, and what is the recommended treatment?
Diffuse large B-cell lymphomaALL with leukocyte count 50,000-100,000/uL (50-100 � 109/L)Acute myeloid leukemia with leukocyte count 10,000-50,000/�L (10-50 � 109/L)Chronic lymphocytic leukemia with Leukocyte count 10,000-100,000/�L (10-100 � 109/L) treated with fludarabineOther hematologic malignancies (including chronic myeloid leukemia and multiple myeloma) with rapid proliferation with expected rapid response to therapy
Treatment: Hydration + Allopurinol therapy
What patients are at Low risk for Tumor Lysis Syndrome, and what is the recommended treatment
Non-Hodgkin lymphoma with indolent non-Hodgkin lymphomaAcute lymphoblastic leukemia with leukocyte count ?50,000/�L (50 � 109/L)Acute myeloid leukemia with leukocyte count ?10,000/�L (10 � 109/L)Chronic lymphocytic leukemia with Leukocyte count ?10,000/�L (10 � 109/L) and solid tumors
What kind of hydration is used to treat tumor lysis syndrome?
Urinary alkalinization has historically been used to treat tumor lysis syndrome but has been shown to increase the risk of calcium phosphate deposition in the renal tubules, leading to worsening kidney dysfunction. Hydration with isotonic saline is therefore preferred.
When is dialysis recommended in tumor lysis syndrome?
What medication is contraindicated in pts with myeloma cast nephropathy and GFR is below 30 mL/min/1.73 m2?
In a chemo patient who is receiving cisplatin, what can you give to attenuate direct tubular toxicity?
What is the treatment for IgA nephropathy?
ACE inhibitor or an ARB is indicated for patients with IgA nephropathy who have good prognostic indicators such as normal kidney function, normal blood pressure, and a urine protein-creatinine ratio less than 1 mg/mg.Those with progressive disease who have elevated serum creatinine levels should receive pulse corticosteroid therapy or, if kidney insufficiency is present, corticosteroids and an alkylating agent.
How do you manage a pt with staghorn calculi?
In patients with staghorn calculi, stone removal is indicated to prevent obstructive nephropathy, loss of kidney function, or pyelonephritis and sepsis. Percutaneous nephrolithotomy is the initial treatment of choice for staghorn calculi, particularly those that are larger than 4 cm in diameter.Extracorporeal shock-wave lithotripsy (ESWL) is associated with a high risk for residual stone fragmentation that may cause future infection and stone growth. Therefore, ESWL is recommended only for patients with stones smaller than 4 cm in diameter and is often combined with percutaneous nephrolithotomy to allow for direct visualization of stone removal.
When does it usually occur?
What is the manifestation?
Typically occurs within the first 2 weeks after drug administration and manifests as a Fanconi-like syndrome of glycosuria, phosphaturia, aminoaciduria, and renal wasting of magnesium and hypomagnesemia.
What is an important point to remember in kidney transplant recipients who had a previous FSGS?
Focal segmental glomerulosclerosis can recur soon after kidney transplantation, sometimes within minutes or hours of this procedure.
How do you manage a pt with a complex kidney cyst?
Surgical resection is indicated for patients with Bosniak category III and IV kidney cysts.
What is adynamic bone disease?
In what group of patients does it occur?
How is it different from bone disease secondary to hyperparathyrodisim?
Adynamic bone disease commonly occurs in patients with ESKD and may cause fractures. However, unlike bone disease associated with secondary hyperparathyroidism, adynamic bone disease is often associated with hypoparathyroidism caused by excess vitamin D intake and/or calcium loading. This condition usually manifests as bone pain accompanied by a serum parathyroid hormone level below 100 pg/mL (100 ng/L) and a normal alkaline phosphatase level.
Explain why pts with ESRD may develop "bone disease due to secondary hyperparathyrodism?
Chronic kidney disease (CKD) is associated with progressive alterations in mineral and bone metabolism that can cause bone disease. In patients with end-stage kidney disease (ESKD), the kidney�s inability to excrete phosphorus leads to hyperphosphatemia. Loss of kidney function also is associated with 1,25-dihydroxyvitamin D deficiency. Hyperphosphatemia along with decreased 1,25 dihydroxy-vitamin D levels result in hypocalcemia, which leads to direct stimulation of parathyroid hormone secretion. Furthermore, decreased 1,25 dihydroxyvitamin D levels cause increased production of parathyroid hormone.
What is adynamic bone disease?
Adynamic bone disease is a major cause of bone disease in patients with stage 5 chronic kidney disease and usually manifests as osteopenia, fractures, and bone pain accompanied by a serum parathyroid hormone level below 100 pg/mL (100 ng/L) and a normal alkaline phosphatase level.
How do you evaluate suspected hyeraldosteronism in a pt with resistant hypertension?
Patients with hypertension should be screened for primary hyperaldosteronism if they are young, have hypokalemia, or have difficult-to-control blood pressure; such screening includes determination of the serum aldosterone to plasma renin activity ratio, with a ratio greater than 20 strongly suggesting the diagnosis. The best screening test for primary hyperaldosteronism is a determination of the ratio of serum aldosterone (in ng/dL) to plasma renin activity (in ng/mL/min). A ratio greater than 20, particularly when the serum aldosterone level is greater than 15 ng/dL (414 pmol/L), is consistent with the diagnosis of primary hyperaldosteronism.After biochemical confirmation of hyperaldosteronism, localization procedures are appropriate to differentiate aldosterone-producing adenomas, which are amenable to surgical resection, from bilateral hyperplasia, which is medically treated. Given the high incidence of incidental adrenal lesions, however, imaging studies, such as CT of the adrenal glands, should not be performed before autonomous production of aldosterone is confirmed through biochemical testing.
How do you manage recurrent uric acid nephrolithiasis?
Alkalinization of the urine with potassium citrate thera;y to obtain a urine pH above 6.0 decreased the risk of recurrent uric acid stones.Consumption of more than 2 L of fluid daily and restriction of sodium inatake are recommended for all patients with a history of nephrolithiasis, and targeted therayp is recommended for patients with a metabolic abnormality that favors stone formation. Because the solubility of uric acid increases in alkaline urine, use of potassium citrate to obtain a urine pH above 6.0 would decrease this patient�s risk for recurrent uric acid stones.
How do you manage a pt with an acute attack of nephrolithiasis?
Kidney stones may take several days to weeks to pass spontaneously. If a stone does not pass within 2 to 4 weeks, rapid stone removal is indicated. This intervention also is recommended for patients with infection, intractable nausea and vomiting, complete obstruction or anuria, and stones greater than 1 cm in diameter. Extracorporeal shock-wave lithotripsy would be warranted in these settings or in a patient with a stone that is less than 1 cm in diameter located within the kidney or higher than mid ureter, which is not consistent with this patient�s presentation. Furthermore, even if stone removal were indicated for this patient, flexible ureteroscopy would be a more appropriate method than extracorporeal shock-wave lithotripsy to remove a stone located in the distal ureter.
When is Extracorporeal shock-wave lithotripsy (ESWL) indicated?
ESWL is indicated for stones less than 1 cm in diameter located in the kidney and upper urinary tract and in conjunction with with percutaneous nephrolithotomy to help break apart large stones or staghorn calculi.
When is percutaneous nephrolithotomy indicated?
Percutaneous nephrolithotomy is indicated for stones larger than 1 cm in diameter, staghorn calculi, and cystine stones that are resistant to ESWL. This intervention also is indicated for patients with urinary tract abnormalities such as horseshoe kidney.
When is ureteronoscopy recommended in the treatment of kidney stones?
It is recommended to remove stone in the distal ureter or to remove stone fragmens caused by ESWL.
What urinalysis result point toward acute tubular necrosis?
What conditions usually point toward the development of ATN?
Elevated serum creatinine level, minimal proteinuria, and muddy brown casts.This condition usually develops after a sustained period of ischemia or exposure to nephrotoxic agents such as cisplatin, intravenous aminoglycosides, or radiocontrast.
When does acute interstitial nephritis commonly develop?
It commonly develops after exposure to certain medications, including bactrim. Manifestations of this condition may include rash, pruritus, eosinophilia, and fever. Urine sediment findings include pyuria, leukocyte casts, microscopic hematuria, and tubular-range proteinuria.
Trimethoprim can increase serum creatinine by how much?
0.5 mg/dL or less
Chronic calcineurin inhibitor nephrotoxicity is characterized by what?
Cyclosporine and tacrolimus, even when present in the serum at nontoxic levels, can cause kidney injury. Chronic calcineurin inhibitor nephrotoxicity is characterized by an elevated serum creatinine level, hyperkalemia, hyperuricemia and gout, and a normal anion gap metabolic acidosis.
How do you diagnose isopropyl alcohol poisoing?
It is characterized by an increased osmolal gap in the setting of positive serum and urine ketones, and does not cause metabolic acidosis
A pt appears intoxicated and unconscious, with elevated osmolal gap. How do you differentiate the causes?
An elevated osmolal gap suggests the presence of an unmeasured osmole and is most commonly caused by ethanol. The osmolal gap is also elevated in the presence of ethylene glycol, methanol, and isopropyl alcohol. However, isopropyl alcohol does not cause an elevated anion gap metabolic acidosis (methanol and ethylene glycol poisoning) and is not associated with retinal abnormalities (methanol poisoning) or kidney failure (ethylene glycol poisoning).
A pt with a history of "glue sniffing (inhalant abuse)" was brought to the ED with MS change. Describe the lab findings that you would expect.
metabolic acidosis, hypokalemia, hypophosphatemia, rhabdomyolysis, and elevated creatine kinase level.