Nephrology

Calculated Osm = 2 (Na) + BUN/2.8 + Glucose/18

Osm gap = Measured - Calculated


Normal OG < 10

• Metabolized to acetone.
• Causes Osmolar Gap and Ketosis, but no AG

• Ingested as antifreeze
• Can cause profound shock
• Anion gap metabolic acidosis, osmolar gap
• Metabolized to calcium oxalate crystals in urine
• Treatment: fomepizole, folic acid, dialysis

Solvent in IV lorazepam, diazepam, and propofol which can cause lactic acidosis

• Loss of HCO3: Diarrhea, Ureteroenterostomy (ileal loops)
• Inability to excrete H+: RTA
• Exogenous Acid: TPN
• -- Addition of lysine, arginine

• Seen in Diarrhea and RTA
• Differentiate the two above by measuring Urine AG
• UAG = (U_Na + U_K) - U_Cl
• Serves as a measure of kidney's ability to generate ammonium
• In non-AG acidosis, calculate UAG:
• Negative UAG = Diarrhea: kidney generates NH_4, urine Cl increases
• Positive UAG = RTA: NH₄ production is impaired

Type 4 or Type 1

Type 2

Type 1 and 2

Type 4

• Can't excrete H+ ions across concentration gradient
• Urine pH never less than 5.5, despite presence of acidemia
• Associated with hypercalcemia, stones, nephrocalcinosis
• Etiologies: Amphotericin, toluene, hypergammaglobulinemia
• Treatment: Potassium and HCO3 replacement, Shohl's solution

• Amphotericin
• Toluene
• Hypergammaglobulinemia

K and HCO3 replacement

• Hypercalcemia
• Nephrolithiasis
• Nephrocalcinosis

• Mechanism: Bicarb wasting
• Urine pH is high early in course, then falls as serum pH falls
• Etiologies: Drugs - CA inhibitors, amphotericin, heavy metals, myeloma, Sjogren's syndrome
• Look for Fanconi Syndrome: hypophos, hypouricemia, glycosuria, AAuria (coal -- cysteine, ornithine, arginine, lysine)
• Treatment: lots of HCO3

• Carbonic Anhydrase inhibitors
• Amphotericin
• Heavy metals
• Myeloma
• Sjogren's syndrome

• Hyperkalemic, hyperchloremic metabolic acidosis
• Mechanism: usually hyporenin, hypoaldo
• Etiology:
• - DM, most common
• - Obstructive uropathy
• - Interstitial renal disease, sickle cell disease
• - Drugs: cyclosporine
• Treatment: HCO3, furosemide, Florinef

• Vomiting: UGI losses
• Diuretics
• Post-hypercapnia
• CF

• Bartter syndrome
• Gitelman syndrome
• Surrptitious diuretics

• Exogenous steroids
• Endogenous steroids
• 1⁰ hyperaldo
• Cushing's
• 11-OH defic
• Liddle syndrome

• Hypokalemia
• Metabolic alkalosis and normal BP
• Low mag, high renin and aldo
• Hypercalciuria
• No chondrocalcinosis
• Defect in the Ascending Loop
• Looks like the pt is taking a loop diuretic
• Rx: NSAIDs, K

• Metabolic alkalosis and normal BP
• Low K, low Mg
• Hypocalciuria
• Associated with Chrondrocalcinosis
• Defect in the Distal Convoluted Tubule
• Looks like the pt is taking a thiazide diuretic
• Tx: Magnesium, K, sometimes amiloride or spironolactone

• Restrict water
• Diuretics

• U_Osm inappropriately high for low S_Osm, low uric acid levels
• Always R/O Addison disease
• Rx: Demeclocycline, Lithium, Vasopressin receptor antagonists (cornivaptan)

• Hereditary: X-linked defect in V2 receptot gene
• Drugs: Lithium, Demeclocycline, Amphotericin
• Electrolytes: Hypercalcemia, hypokalemia
• Sjogren's

Thiazides

• Amiloride
• Thiazides
• NSAIDs

• Peaked T waves
• Widened QRS
• Loss of P waves
• Bradyarrhythmias

• CKD
• Hypoparathyroidism
• Pseudohypoparathyroidism
• Hypomag
• Acute Pancreatitis
• Rhabdomyolysis
• Vitamin D Deficiency

• 1. Endo causes:
• - High PTH
• - Hyperthyroidism
• - Addison's
• 2. Granulomatous Dis -- Sarcoid, TB
• 3. Malignancy
• 4. Toxicity -- Vitamin A or D, Thiazides, Milk-Alkali syndrome
• 5. Familial Hypocalciuric Hypercalcemia

"The Amish Pay Cash for their Penthouse"

• Thiazides
• Aminoglycosides
• Cisplatinum
• Cyclosporine
• Pentamidine

• Alcoholic Ketoacidosis
• DKA
• Refeeding/Hyperal
• Phosphate binders
• HyperPTH

• Hemolysis, Thrombocytopenia, Poor WBC function
• Rhabdo
• Muscle paralysis

• Works in the proximal tubule
• Causes a Type II RTA
• Causes a metabolic acidosis, so used for treatment of met. alkalosis, mountain sickness, glaucoma

• Inhibit Na-K:2Cl channel
• Useful in hypercalcemia, Type 4 RTA

120-130/80-89

140-159/90-99

≥160 / ≥100

• There is high cortisol, low renin and low aldosterone.
• Glycyrrhizic acid also inhibits 11-hydroxysteroid dehydrogenase

• HTN with low K and metabolic alkalosis
• Abnormality is in salt absorption
• Defect in the amiloride sensitive Na channel results in chronic volume expansion
• Low renin, Low aldo levels
• Autosomal dominant
• Treatment: triamterene and Na restriction

• <150 mg/day
• < 200 mg/g (.2) in a spot urine

• TB
• prostatitis
• analgesic abuse nephropathy

• RBC casts
• Proteinuria
• Elevated creatinine

• 1. Glomerulonephritis
• 2. Pyelo
• 3. Interstitial inflammation
• 4. ATN
• 5. CKD

• UA
• FEN
• U/S of kidney
• Renal bx if ARF unresolved or unexplained

• Always consider when ARF occurs with patient on a new medication
• Clinical clues: rash, fever, eosinophilia
• UA: renal tubular cells +/- casts
• Eosinophils in the urine (Wright or Hansel stain)

• NSAIDs
• Antibiotics: PCN, sulfa, cephalosporins, rifampin, quinolones

• May occur months after beginning NSAID in patients with normal renal fxn
• AIN with nephrotic range proteinuria
• This is different than the pre-renal ARF that NSAIDs cause in patients with pre-existing renal disease

• ATN
• Muddy brown cast

• DM
• CKD
• CHF

• .9 NS 1 ml/kg/kg for 24 hour
• Low osmolality contrast, lowest dose
• Prevention: N-acetylcysteine, NaHCO3
• Stop metformin, diuretics, NSAIDs

*Please note that this is an exception -- FE_Na may be low

• ARF or CKD with GFR < 30 ml/min
• ARF due to hepatorenal syndrome or post-op liver transplant

• Tightening of the skin of trunk and extremities, unlike scleroderma, spares face.
• May affect internal organs

• Presentation: Sudden onset, severe nephrtoic syndrome
• Most common in children, but 10-15% of adult cases of NS
• Usually GFR is normal, no HTN
• Most cases are idiopathic
• May be caused by NSAIDs, also assoc with Hodgkin Disease
• Treatment: steroids, especially in children, may need cytotoxics in adults

Foot process fusion along the GBM seen on EM

• Most common cause of idiopathic nephrotic syndrome in African-Americans
• Frequently associated with reduced GFR, HTN and progressive renal failure
• Most common etiology is idiopathic
• - HIV-associated Nephropathy
• - Reflux nephropathy
• - Obesity
• Tx: ACE-I, ARB, steroids

• Suspect Primary (AL) Amyloidosis
• Usually rapidly progress to end-stage disease
• Associated with overproduction of light chains
• Assoc with other organ involvement, i.e., hepatomegaly, restrictive CMP
• Diagnosis: SPEP, UIEP, Biopsy
• Responds poorly to treatment

• Secondary Amyloidosis
• In FMF, colchicine prevents amyloidosis
• Always consider MM as etiolgy
• Rate of progression slowed with eprodisate

colchicine

eprodisate

• 1⁰
• Post-infectious GN
• MPGN

• 2⁰
• SLE
• Endocarditis
• Cryoglobulinemia

• 1⁰
• ANCA (+) RPGN
• IgA Nephropathy
• Alport syndrome

• 2⁰
• Goodpasture's
• Vasculitis
• TTP/HUS

• Proteinuria
• Hematuria
• ± RBC casts
• Reduced GFR
• Salt and water retention

• 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 strep
• Most commonly presents with gross hematura
• Labs:
• ASO positive
• C3 falls and returns to normal after 6-8 weeks
• Generally self-limited

Subepithelial humps on EM, which are immune complexes

• Proteinuria -- 100%
• Nephrotic syndrome -- 45 - 65%
• RBC casts -- 10%
• Microscopic hematuria -- 80%
• Decreased GFR -- 40-80%

• I Normal Glomeruli
• II Mesangial
• III Focal proliferative
• IV Diffuse proliferative
• V Membranous

Steroids with cyclophosphamide or MMF

• Steroids for Mesangial lupus nephritis
• Pulse steroids and cyclophosphamide, or later MMF, or just MMF and steroids for Proliferative lupus nephritis

• Typically associated with HCV
• Clinical presentation: purpuric skin lesions, polyarthralgias, glomerulonephritis
• Labs: C4 low, RF +, "mixed" IgG-IgM cryoglobulins+
• 25% will be mixed "nephritic" and "nephrotic"
• Renal disease may improve with treatment of HCV, relapses common

• purpuric skin lesions
• polyarthralgias
• glomerulonephritis

• C4 low
• RF +
• "mixed" IgG-IgM cryoglobulins+
• 25% will be mixed "nephritic" and "nephrotic"

Histologic hallmark is the "crescent"

• 1. ANCA (+) = Pauci-immune GN (No immune deposits)
• 2. Anti-GBM Antibody disease
• - Goodpasture Syndrome
• - Idiopathic Anti-GBM Ab GN
• 3. Immune Complex-Mediated RPGN
• - SLE, Post-infectious GN (some cases only)
• - IgA Nephropathy

• Presents as insidious, rapidly progressive GN with HTN
• Represents a "microscopic" polyangiitis
• Serology (-) except ANCA
• Requires urgent renal bx: Only finding is extracapillary proliferation -- "crescents"
• Treatment: "pulse" methylprednisolone, cyclophosphamide

IgA Nephropathy

• Very common form of GN world-wide
• Typically presents with gross hematuria immediately after URI
• Pts frequently have normal GU eval before referral for renal biopsy
• Rare in Af-Am
• Progressive renal failure in some patients, especially if severe proteinuria and/or hypertension

kidney biopsy

• Hereditary nephritis: Alport Syndrome
• Familial renal disease, usually X-linked
• Patients typically present with hematuria immediately following URI (lack of latent period distinguishes from Post-Strep GN)
• Ocular disorders may be associated
• Primary abnormality is defect in alpha-5 subunit of Type IV collagen

• 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

• Anti-GBM antibodies, acute GN, pulmonary involvement
• Usually present with hemoptysis, dyspnea
• Treatment: Plasmapheresis, high-dose steroids

• Goodpasture Syndrome
• Wegener granulomatosis
• Lupus and other vasculitides
• Infcetious endocarditis (right sided)
• Sarcoidosis

Anti-GBM antibodies

• Affects medium-sized arteries, multi-system involvement
• Renal involvement due to renal aneurysms leading to renal ischemia/infarction

Celiac arteriogram

• "pulse" steroids
• cytotoxic drugs

• 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

• granulomas on biopsy
• vasculitis
• C-ANCA (+)

Thrombotic microangiopathy

• Complement levels
• ANA
• Hepatitis studies
• ANCA
• Blood Cx
• Lupus studies
• ASO titers
• Anti-GBM antibodies
• And finally, Renal biopsy

Plasmapheresis

• Chronic interstitial nephritis with little proteinuria
• May present with acute flank pain due to papillary necrosis
• Will have sterile pyuria
• Imaging shows papillary necrosis
• Can be contributed to by Tylenol

• sickle cell disease
• DM with pyelo

• Not done routinely
• It is recommended for those with PCKD with symptoms suspicious for aneurysm and those with family history of PCKD and aneurysms

• Monitor for Renal Osteodystrophy
• Screen for secondary hyperparathyroidism
• Monitor calcium and phosphorus
• Measure iPTH
• Alk phos may be elevated
• Goal is to keep Ca X Pho < 55

750 - 1000 mg/day

• Dietary restriction of phosphorus (750-1000 mg/day)
• Ca-containing phosphate binders: Calcium CO₃ or Calcium acetate
• Sevelamer or lanthanum
• Al (OH)₃

• Measure serum 25-OH Vitamin D level
• 1, 25 Vit D₃ (calcitriol) or Vit D analogues (zemplar, Hectorol)
• Calcimimetic agent - Cinacalcet

Parathyroidectomy

• Goal Hgb is 11-12
• If Hgb is < 11, check for iron deficiency with Fe TIBC, Sat and Ferritin
• Target ferritin value is >100
• Target Iron saturation >20%
• If Hgb < 11, give erythropoietin

• It may exacerbate anorexia and bone disease.
• Keep serum HCO3 > 20

• Pericarditis
• Encephalopathy

PD fluid WBC count > 100 with > 50% PMNs

IP Vancomycin or cefazolin and ceftazidime/cefepime (or gentamicin)

• Triple therapy
• Prednison
• Cyclosporine or tacrolimus and/or sirolimus
• Celcept

• Bactrim
• Ganciclovir

• "D-A-V-E-C"
• erythromycin
• clarithromycin
• verapamil
• diltiazem
• azole anti-fungals

• rifampin
• phenobarb
• phenytoin

• high dose steroids
• Polyclonal or monoclonal antibodies

• Kidneys enlarge
• Salt and water retention occur
• Serum Na falls, BUN falls
• Respiratory alkalosis
• Uric acid falls, can have renal glycosuria
• SVR falls: BP falls, normal always < 120/80
• GFR rises: normal Scr < 0.8 mg/dL

• HTN and proteinuria beginning after the 20th week of pregnancy
• Edema no longer part of the definition
• If these sx occur in early pregnancy, suspect underlying chronic renal disease

• Hemolysis
• - abnormal peripheral smear
• - bilirubin > 1.2
• - LDH > 600
• Elevated LFT
• - AST > 70
• Low Platelets: < 100,000

• Primigravida (> 50%)
• fever
• abdominal pain
• nausea and vomiting
• after 35th week

• Exam: jaundice, HTN, edema, abdominal pain
• Lab: hyperbiliruvinemia, mild elevation of transminases, hepatic/renal failure

termination of pregnancy

• Idiopathic Post-Partum Renal Failure
• Clinical Features:
• - Microangiopathic hemolytic anemia
• - Renal thrombotic microangiopathy
• - Acute renal failure
• - Malignant HTN
• - Thrombocytopenia
• Begins days to weeks following a normal pregnancy
• Treatment: usually plasma exchange, ? steroids

• All patients
• - increase water intake, reduce protein
• - increase diet vegetables and fruit
• - Reduce dietary NaCl
• Hyercalciuria -- treat with HCTZ
• Hypocitraturia -- treat with K-citrate
• Hyperocaluria -- diet, pyridoxine
• Hyperuricosuria -- allopurinol

• Hyperuricosuria?
• - reduce dietary purines
• - allopurinol
• Persitently acid urine
• - KHCO3, K citrate, NaHCO3 to keep urine pH > 6.5 - 7
• - Reduce dietary protein
• Chronnic volume depletion: chronic diarrhea
• - correct it

• Triple phosphate crystals that have coffin lid appearance
• Usually due to recurrent UTI caused by urease splitters, i.e., proteus, providencia, klebsiella
• Urolotic removal of stone
• Appropriate antibiotics

• Keep urine output > 2.5 - 3 L/day
• KHCO3 to keep urine pH > 7 - 7.5
• Treatment: D-penicillamine or tiopronin
• -- forms more soluble mixed disulfides with cysteine that are more soluble than cysteine

• Octagonal
• Look like "Stop signs."

• Hypocomplementemia
• Dysmorphic erythrocytes
• Erythrocyte casts seen on urinalysis

Associated with HIV infection, syphilis, Hep C, or any chronic infection

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.

A diagnosis of rhabdomyolysis should be considered in patients with a serum creatine kinase level above 5000 U/L (83.5 µkat/L) who demonstrate heme positivity on urine dipstick testing in the absence of hematuria

• Hypocalcemia
• Hyperphosphatemia
• Hyperuricemia
• Metabolic acidosis
• Atue muscle compartment syndrome
• Limb ischemia

• BP target in pts with ADPKD is less than 125/75
• Frontline med is ACE-I or ARB

• 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.

• Small kidney size
• Absence of HTN or proteinuria

intra-arterial digital subtraction angiography

A transferrin saturation below 20% and a serum ferritin level below 100 ng/mL (100 µg/L) are diagnostic of iron deficiency in predialysis patients with CKD.

• Chemo and plasmapheresis
• Dialysis also if with symptomatic uremia

• volume expansion
• alkalinization of the urine
• discontinuation of nephrotoxic agents
• avoidance of radiocontrast agents

• It is caused by urate deposition and calcium phosphate ppt within the renal tubules
• Develop after initiation of chemo and can occur spontaneously in pts with a hign tumor burden
• Can manifest as acute oliguric kidney injury accompanied by increased serum uric acid, phos, and potassium levels

• High risks are:
• 1. Burkitt lymphoma
• 2. NHL lymphoblastic
• 3. Burkitt acute lymphoblastic leukemia
• 4. ALL with leukocyte count ≥100,000/uL
• 5. AML with leukocyte count ≥50,000/uL
• 6. serum uric acid levels higher than 7.5 mg/dL (0.4 mmol/L)

Treatment: Hydration + Allopurinol + rasburicase

• Diffuse large B-cell lymphoma
• ALL with leukocyte count 50,000-100,000/uL (50-100 × 10⁹/L)
• Acute myeloid leukemia with leukocyte count 10,000-50,000/µL (10-50 × 10⁹/L)
• Chronic lymphocytic leukemia with Leukocyte count 10,000-100,000/µL (10-100 × 10⁹/L) treated with fludarabine
• Other hematologic malignancies (including chronic myeloid leukemia and multiple myeloma) with rapid proliferation with expected rapid response to therapy

Treatment: Hydration + Allopurinol therapy

• Non-Hodgkin lymphoma with indolent non-Hodgkin lymphoma
• Acute lymphoblastic leukemia with leukocyte count ≤50,000/µL (50 × 109/L)
• Acute myeloid leukemia with leukocyte count ≤10,000/µL (10 × 109/L)
• Chronic lymphocytic leukemia with Leukocyte count ≤10,000/µL (10 × 109/L) and solid tumors

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.

• oliguric
• life-threatening hyperkalemia

Oral bisphosphonates

theophylline

• 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.

• 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.

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.

Focal segmental glomerulosclerosis can recur soon after kidney transplantation, sometimes within minutes or hours of this procedure.

Surgical resection is indicated for patients with Bosniak category III and IV kidney cysts.

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.

• 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.

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.

• 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.

• 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.

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.

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.

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.

It is recommended to remove stone in the distal ureter or to remove stone fragmens caused by ESWL.

• 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.

• 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.

0.5 mg/dL or less

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.

• It is characterized by an increased osmolal gap in the setting of positive serum and urine ketones, and does not cause metabolic acidosis

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).

metabolic acidosis, hypokalemia, hypophosphatemia, rhabdomyolysis, and elevated creatine kinase level.