GU

• Rapidly deteriorating GFR with accumulation of nitrogenous wastes (azotemia)
• Serum Cr increases b more than 0.5 mg or more than 50% over baseline levels

• N/V/D
• Pruritus
• Drowsiness, dizziness, hiccups, SOB, anorexia, hematochezia

• Tachycardia and hypotension in prerenal
• Distended bladder, CVA tenderness, enlarged prostate in postrenal
• Anuria or oliguria, change in volume status, change in MS, edema, weakness, dehydration, rashes, JVD, urinerferous odor, ecchymosis

GFR

BUN/Cr

• dehydration
• catabolism
• diet
• renal perfusion
• liver disease

nl with few hyaline casts

NL with few hyaline casts

• Urine Na < 20
• FENa < 1%
• Urine osmolality 500 mOsm
• Elevated BUN/Cr ratio (20:1)

< 10 cm

• Increased urine Na > 40 mEq/L
• FENa > 1-2%
• Urine mOsm 250-300
• Decreased BUN/CR ratio

When CR exceeds 5-10 mg

• AEIOU
• Acidosis
• Electrolyte imbalance
• Increase Cr
• Overload fluid
• Uremia

• Stage 1: GFR > 90; asx
• Stage 2: GFR 60-89; asx
• Stage 3: GFR 30-59; asx, BUN/Cr increase
• Stage 4: GFR 15-29; sx (anemia, acidosis, ^K, vCa, ^phosphatemia)
• Stage 5: GFR < 15; candidate for kidney transplant

DM (m/c), HTN, GN, PCKD

• Fatigue, malaise, anorexia
• N/V
• metallic taste, hiccups
• dyspnea, orthopnea, impaired mentation
• insomnia, irritability, muscle cramps, restless legs
• weakness, pruritus, easy bruising, altered consciousness

Deep forced, labored breathing with increasing intensity

GFR via Cockcroft-Gault formula

• Proteinuria if kidney damage, microalbuminuria early
• increased BUN/Cr
• Hgb, Hct, electrolytes, and UA are abnl

• ACE-Is and ARBs to slow progerssion of renal dysfucntion
• tight HTN and glycemic control
• LDL < 100, tobacco cessation, weight control
• EPO, iron supplements, antiplatelet therapy
• Restrict protein intake, adequate caloric intake, Ca and Vit D supplements, limitation of water, Na, K, and phos

damage of the renal glomeruli by deposition of inflammatory proteins in the glomerular membranes as the result of an immunologic response

Children: benign hematuria, HSP, mild post-infectious GN, IgA nephropathy, hereditary nephritis, membranoproliferative GN

Adults: IgA nephropathy, hereditary nephritis, SLE, post infectious GN, vasculitis

diffuse > 50% of glomeruli affected

• Hematuria, tea or cola colored urine
• Oliguria or anuria
• Edema of face and ees in the morning, feet and ankles in the afternoon and evening
• HTN is common

• Antistreptolysin O titer increased in 60-80%
• UA shows hematuria, with misshaped RBCs (acanthocytes); RBC casts, and proteinuria (1-2g/24 hours)
• Decreased C3

• Steroids and immunosuppressive drugs
• Decrease salt and fluid intake
• Dialysis if symptomatic azotemia is present
• Medical therapy: ACE Is in chronic GN; tx other sx as necessary

• Excretion of more than 3.5g protein  in 24 hours
• manifests with hypoalbuminemia, lipiduria, hypercholesterolemia, and edema

secondary to loss of proteins S and C and antithrombin III

malaise, abdominal distention, anorexia, facial edema/puffy eyelids, oliguria, scrotal swelling, SOB, weight gain

ascites, edema, HTN, orthostatic hypotension, retinal sheen, skin striae

• UA shows proteinuria, lipiduria, glycosuria, hematuria, and foamy urine
• UA also shows RBC casts, granular casts, hyaline casts, fatty casts, oval fat body **** (renal tubular cell that has reabsorbed some of the excess lipids in urine)
• Blood shows: hypoalbuminemia, azotemia, HL

liver producing increased lipoproteins d/t hypovolemia from the loss of intravascular volume

• Any sort of glomerular disease state
• SLE
• malignancy
• toxemia of pregnancy
• drugs and nephrotoxins
• lymphomas and leukemias
• DM
• amyloidosis

• ACE-Is early
• diurectics to reduce fluid
• restrict Na and fluid intake
• Nl protein and K, but not excessive
• Tx infections
• anticoagulants if thromboses are present
• some pts need steroids

• aminoglycosides
• NSAIDs

growth of cysts made of epithelial cells from the renal tubules and collecting system, that replace the mass of the kidneys, reducing function and leading to kidney failure

autosomal dominant, B/L

• back and flank pain, HA
• Hematuria, HTN, recurrent UTI, weight loss, renal colic, N/V

• anemia
• UA shows protienuria, hematuria, pyuria, bacteriruia

U/S

• supportive
• manage pain, control HTN, intake of fluids, low-protein diet
• Tx infections vigorously with abx (bactrim, quinolones, chloramphenicol, vanco)
• dialysis or transplant when needed

calcium, they are radiopaque

radiolucent

radiolucent

formed by combo of Ca, ammonium, amd magnesium and are radiopaque

• < 5 mm: may pass spontaneously, manage on an outpt basis, drink plenty of fluids, strain urine
• 5-10mm: elective lithotripsy or uteroscopy with stone basket extraction
• >10mm: tx on inpt basis, vigorous hydration, ureteral stent or percutaneous nephrostomy, analgesics, lithotripsy

• inpt
• administer free water
• dialysis if Na > 200

can cause pulmonary or cerebral edema, esp. in pts with DM

<125

hyponatermia

• CHF
• nephrotic syndrome
• renal failure
• hepatic cirrhosis

• hypothyroidism
• glucocorticoid excess
• SIADH release

hypotonic hyponatermia, urine osmolality > 100 mOsm, nl cardiac, hepatic, thyroid, adrenal, and renal funciton; absence of extracellular fluid volume deficit (Urine Na > 40 mEq/L)

occurs with renal or nonrenal Na loss

CT to r/o CNS disorder; CXR to r/o lung pathology

• tx hyponatremia on inpt basis
• tx underlying cause
• monitor volume status

overly rapid correction of hyponatremia with hypertonic saline

caused by deficienct secrtion of arginine vasopressin (ADH) from posterior pituitary

Caused by kidneys unresponsive to nl vasopressin levels; may be inherited x-linked disorder or acquired as a result of lithium therapy, hypokalemia, hypercalcemia, or renal dz

parenteral or intranasal desmopressin

HCTZ or amiloride diuretics or indomethacin

• renal failure, ACE-Is, hyporeninemic hypoaldosteronism, cell death, and metabolic acidosis
• also hemolysis or thrombocytosis

numbness, tingling, weakness, flaccid paralysis

• K > 5
• measure BUN and Cr
• decreased FE-K

• >6.0
• earliest manifestation is peaking of the T waves
• flattening of the p wave, prolongation of PR interval, widening of QRS in > 7
• Final event is sine-wave pattern with cardiac arrest (8.0 to 10)

• Stop K sparing drugs and K supplements, low K diet
• If severe with EKG changes, calcium gluconate via IV to antagonize the effects of ^K on the heart
• Sodium bicarb, glucose (D50), and insulin to drive K back into the intracellular compartment
• Kayexalate to remove K when levels are extremely high
• dialysis if everything fails

• shift of K into intracellular compartment, of from K losses of extrarenal or renal origin
• m/c caused by diuretics, renal tubular acidosis, or GI loss

• K < 3.5
• EKG shows flattened or inverted T waves, increased prominence of U waves, depression of ST segment, and ventricular ectopy

• no tx needed unless cardiac manifestations are present
• PO KCl therapy
• aggressive K replacement in cardiac glycosides, as it can lead to dig intoxication

• parathyroid disorders
• chronic renal failure
• malignancy

malignancy (lung cancer, squamous cell carcinoma of head and neck, esophagus) vit D intoxication, hyperparathyroidism, and sarcoidosis

asx until > 12

malignant neoplastic or paraneoplastic process or hyperparathyroidism

primary hyperparathyroidism

isotonic saline, loop diuretics, manage underlying cause

CKD

<8.5

• tx any emergent cardiovascular states
• replace severe deficiency with clacium gluconate or calcium chloride

CKD

• initially reduced DTRs
• muscle weakness, hypotension, respiratory depression, then cardiac arrest
• N/V/flushing

widened QRS complex, prolonged PR interval, prolonged QT interval

• 10-20 mL of 10% calcium gluconate IV over ten minutes
• saline diuresis and IV furosemide may increase excretion of magnesium
• dialysis if severe

• chronic alcoholism
• chronic diarrhea
• hypoparathyroidism
• hyperaldosteronism
• diuretic therapy
• osmotic diuresis
• nutritional deficiencies

<7.2, > 7.6

primary increase in pp of CO2 i the blood and decreased blood pH; the kidneys therefore slowly increase bicarb

• failure of lung to excrete CO2
• result of alveolar hypoventilation leading to pulm CO2 retention or of overproduction of CO2 or a combo of both

• primary pulm dz
• myasthenia gravis
• primary CNS dysfunction
• drug induced hypoventilation

2-5 days, when they increase H+ secretion and bicarb production in the distal nephron, after which the plasma bicarb level steadily increases

• tx underlying causes
• ventilation if CNS or pulm depression is severe

decreased blood pCO2 and increased blood pH

• resulve of excessive elimination of CO2 d/t increased ventilatory drive
• kidneys respond to eliminate bicarb

• anxiety m/c
• ASA intoxication
• hypoxia
• intrathoracic disorders
• primary CNS dysfunction
• GM (-) septicemia
• liver insufficiency
• pregnancy

• frequent, deep, sighing respirations to stustained and obvious rapid, deep breathing
• circomoral paresthesias, acropharesthesias, giddiness or lightheadedness

• loss of CO2 via lungs, increase in pH
• within hours H+ secretion in distal nephron decreases, Cl increases

correct underlying disorder

metabolic encephalopathy (aka hypercapnic encephalopathy) with HA and drowsiness is m/c change

• elevation in nl serum concentration of H ions that is initiated by either the loss of bicarb from or by the addition of H+ ions to the serum
• presiratory response is imemdiate with compensatory increase in respiration

• Anything that can cause increased H+ in the blood
• lactic acidosis
• diabetic keotacidosis
• starvation ketosis
• ethlene glcol
• metahol
• salicylate intoxication
• renal tubular acidosis
• renal insufficiency
• adrenal insufficiency

• hyperventilation is earliest
• ventricular arrhythmias
• neurologic sx ranging from lethargy to frank coma)

• bicarb follws the bPh in metabolic acid0base disorders; in acidosis the pH and bicarb both go down
• pH < 7.38m decreased plasma bicarb, decreased pCO2

• tx the cause
• insulin therapy and volume repletion for diabetic ketoacidosis
• Bicarb therapy if pH <7.2

• increase in serum bicarb with no change in PCO2
• kidneys fail to excrete excess HCO3, thereby maintaining the alkalosis

• vomiting
• hyperalimentation therapy
• disproportionate loss of chloride
•  (diarrhea)
• ng tube suciton
• villous adenoma
• chloride diarrhea
• diuretics
• hypercalcemia
• milk-alkali syndrome

• neurologic abnormalities (paresthesias, carpopedal spasm, light headedness)
• volume depletion sx

• interventions to increase renal excretion of bicarb most effecitve
• chloride-responsive conditions (gastric fluid loss, diuretic) tx with solutations containing sodium chloride
• chloride resistant )eg, mineralcorticoid excess) can be tx by removing an adrenal adenoma, or by using spirinolactone

• immunocompetent: tx with quinolones or Bactrim for 1-2 weeks
• hospitalize if severe infections or complicating factors
• f/u urine cultures mandatory 1-2 weeks following treatment

acute prostatitis

• hospitalization for acute
• IV amp and gent until cultures are available and pts are afebrile for 24-48 hours
• Men < 35 yo, ofloxacin x 10 days or ceftriaxone 250 mg IM followed by 10 days of doxy is recommended
• >35 yo,
• NSAIDs for analgesia

testicular swelling and tenderness, usually U/L, with fever and tachycardia

ascending bacterial infection from urinary tract, or in males with mumps

• if mumps, sxmatic relief with ice and analgesia
• bacteria: tx like epididymitis

• <35: G+C
• >35: E coli

• heaviness, dull aching discomfort in the affected hemiscrotum radiating up into the ipsilateral flanks
• markedly swollen and TTP epididymitis
• fever and chills

relief of pain with scrotal elevation with epididymitis

• <35 yo: ceftriaxone 250 mg IM plus doxy 100 mg PO QD x 10 days
• >35: cipro 500 mg PO QD x 10-14 days

peripheral zone

prostate Ca

• Low grade tumors that are well differentiated may not need any therapy
• stage A and B (tumor confined to prostate) tx with radical retropubic prostatectomy, brachytherapy, or external beam radiation therapy
• Stage C disease (tumor with local invasion) tx as A and B, but with reduced effectiveness
• Stage D disease (metastic) hormonal manipulation using orchiectomy, antiandrogens, luteinizing hormone-releasing agonists, or estrogens

RCC

hereditary RCC

• gross or microscpoic hematuria
• gross hematuria, flank pain, and palpable mass is classic triad

• normochromic anemia
• elevated ESR
• hematuria
• dx with CT

• radial nephrectomy for localized dz (T1-T3a)
• radiation therapyy for palliation in pts with disseminated disease
• a-interferon and interluekin to stop growth

Wilms' tumor

Wilms' tumor

• asx abdominal mass found by a family member or during PE
• other sx: anorexia, N/V, fever, abdominal pain, hematuria
• HTN can occur d/t elevated renin levels

• multimodal: surgery, chemo, some radiation
• chemo responsitive to vincristine, , doxorubicin, and dactinomycin

• nonseminomatous
• m/c tpe of nonseminomatous is mixed cell type

AFP or aHCG

mass of fluid-filled congenital remnants of the tunica vaginalis, usually resulting from a patent processes vaginalis

palpable, round, firm cystic mass with distinct borders, free floating above the testicle, which transilluminates, mass may be tender

6 hours

doppler sonography

scrotal/testicular development

chronic kidney disease

medullary sponge disease

proteus

minimal change disease

struvite

staph