☉Cockroft-Gault Formula:	(140-Age)/Cre * BW/72 * Female(0.85)（青春期/平常分） ←→maximal heart rate: (220-Age)* 0.85 （運動太激烈叫餓餓很平常）
☉Tubuloglomerular feedback (TGF):	1.High concentration of NaCl inside DCT stimulates Macula Densa and leads to afferent arteriole constriction and decrease of glomerular filtration rate (GFR, or single-nephron GFR, SNGFR). 2.High concentration of NaCl inside DCT inhibits rennin release from the adjacent juxtaglomerular cells. 3.Decrease of GFR or SNGFR by the activity of Macula Densa (from 1) results in decrease of the concentration of NaCl inside DCT, therefore, increases rennin release and increases blood pressure and Na+/H2O reabsorption by aldosterone, brings the decreased GFR/SNGFR back to normal. 4.The dynamic feedback process regulates and maintains the relative stable GFR/SNGFR
	AG= Na-Cl-HCO3; Osm= 2*Na+ Glu/18 +BUN/2.8
☉ARF:	prerenal: BUN/Cr> 20, Cr U/P> 40, OsmU >350, FENa< 1% （血蛋(BUN)多，尿雞(Cr)鴨(OsmU)多，尿卻那(Na)麼少） renal: BUN/Cr: 10-15, Cr U/P< 20, OsmU =300, FENa> 1%
☉ARF: renal cause	1.Ischemic/ Vascular: ATN 2.Drug: →b-lactam, thiazide, NSAID: ★AIN →★Aminoglycoside(Non-oliguria type!!), Amphotericin B: ATN →Contrast: ATN(DM,MM, ★24hr 後發生,4-10日恢復) →C/T: ATN 3.Metabolic: →hemolysis/hemolytic uremic syndrome, rhabdomyolysis →Ca: ★nephrogenic DI →Urate 4.Immune →Goodpasture's syndrome: anti-glomerular basement membrane(GBM) antibodies, linear deposition of immunoglobulin and complement in GBM, causing pulmonary hemorrhage with severe and progressive glomerulonephritis, attacking noncollagenous (NC-1) domain of the 3 chain in type IV (basement membrane) collagen →ANCA associated: anti-NEUTROPHIL cytoplasmic Ab, WG, polyarteritis →P-ANCA antigen: Myeloperoxidase
☉AD-PCK:	gross hematuria, HTN, UTI,palpable kidney, hepatic cysts, intracranial Berry aneurysm (multiple renal cysts不等於PCK)
☉Alport Syndrome (AS):	defect in basement membranes(Collagen) of the kidney, eye and ear.leakage of small amounts of blood or protein into the urine during childhood
☉Nephrotic syndrome:	LDL, TG...↑HDL不變, antithrombin III↓, encapsulated bac.
☉PSGN:	A beta hemolytic Strept.
☉IgA nephropathy	→immunofluorescence microscopy of granular deposits of IgA and complement 3 (C3) in the glomerular mesangium →Recurrent macroscopic hematuria, usually associated with an upper respiratory tract infection or, less often, gastroenteritis: 50% →asymptomatic, with erythrocytes (RBCs), RBC casts, and proteinuria discovered on urinalysis: 40%
☉Diabetic Nephropathy	Acellular nodules of diabetic glomerulosclerosis (Kimmelstiel-Wilson lesion).
☉Cryoglobulinemic GN:	H"C"V related
☉CRF:	protein 0.6 g/kg/day (s/p H/D=1.2)
☉complications during dialysis	1.Low blood pressure (hypotension). This is the most common complication of hemodialysis. 2.Muscle cramps. If cramps occur, they usually happen in the last half of a dialysis session. 3.Irregular heartbeat (arrhythmia). 4.Nausea, vomiting, headache, or confusion (dialysis disequilibrium). 5.Increase risk of infection, especially if a central venous access catheter is used for hemodialysis. 6.Technical complications, such as trapped air (embolus) in the dialysis tube. 7.Long-term complications of dialysis may include: Inadequate filtering of waste products (hemodialysis inadequacy). Clotting of the dialysis graft or fistula.
☉Hypocalcemia in DM	1.exogenous glucose↓: hunger 2.insulin-independent glucose utilization rate↑: exercise 3.endogenous glucose↓: alcohol
☉Non-anion gap metabolic acidosis:	1.Diarrhea 2.RTA: Type 1, Distal: defect in urine acidification: urinary tract obstruction, Ampho B Type 2, Proximal: defect in bicarbonate reabsorption: myeloma, renal TX Type 3, combination of type 1 and type 2 Type 4, results in high levels of potassium →When potassium levels in the blood are low, as occurs in types 1 and 2, neurologic problems may develop, including muscle weakness, diminished reflexes, and even paralysis. In type 4, potassium levels typically increase, although it is uncommon for the level to rise high enough to cause symptoms. If the level becomes too high, irregular heartbeats and muscle paralysis may develop. →In type 1, kidney stones may develop, causing damage to kidney cells and, in some cases, chronic kidney failure. →A doctor considers the diagnosis of type 1 or type 2 renal tubular acidosis when a person has certain characteristic symptoms (muscle weakness, diminished reflexes) and when tests reveal high levels of acid and low levels of bicarbonate and potassium in the blood. Type 4 renal tubular acidosis is usually suspected when high potassium levels accompany high acid levels and low bicarbonate levels in the blood.
☉cyanide:	nitrite as antedote nitrite causes methemoglobulinemia(blue baby)(chocolate brown), methylene blue as antedote
☉K:	與H, BS同進同出，與beta blocker同調
☉SIADH	（與尿崩症相對比）：低血鈉，水中毒，比較像renal ARF → Ectopic secretion of AVP has been documented from neoplasms and pulmonary tissue. Intracranial lesions likely stimulate AVP release from the neurohypophysis, as do some drugs (e.g. chlorpropamide, vincristine, carbamazepine). Other medications (e.g. chlorpropamide, NSAIDS) potentiate the antidiuretic action of secreted AVP. → Excess AVP secretion or action results in concentrated urine (Uosm > 300 mOsm/kg), low Sosm (Uosm > Sosm), low serum sodium. Urine sodium is usually above 20 mmol/L due to volume expansion inhibiting proximal tubule sodium reabsorption, increased GFR, ★suppression of the renin-angiotensin-aldosterone system, and increased production of atrial natriuretic peptide. This naturiesis tends to normalize extracellular fluid volume. →Urine sodium may be below 20 mmol/L if sodium intake is low. Blood urea nitrogen (< 10 mg/dL) and uric acid (< 4 mg/dL) concentrations are low due to plasma dilution and increase in excretion of nitrogenous compounds. →Clinically significant edema is not present. Extracellular hypotonicity leads to intracellular edema, and severe symptoms may result from cerebral edema. Intracellular fluid volume is reduced after 48 hours by extrusion of osmoles (potassium, creatinine, glutamate, glutamine, taurine, myoinositol, glycerophosphorylcholine). →hypertonic (3%) saline (300-500 mL IV over 4-6 hr), simultaneous administration of furosemide
☉Hypercalcemia:	1.Hyperparathyroidism: primary/tertiary due to CRF 2.Paraneoplastic syndrome: PTHrp, IL-1(NOT PTH!!), eg. MM, SCC...PTH↓↓ 3.Vit D intoxication: PTH↓↓ 4.Granuloma, TB: 1-a hydroxylase→→Vit D activation
☉Cause of hyperuricemia:	1)Increased urate production alcohol(purine-rich food), Myeloproliferative and lymphoproliferative disorders. cytotoxic drugs hyperlipidemia (2)Decreased renal excretion of urate CRI, HTN Drug: cyclosporine (Sandimmune), thiazides, furosemide (Lasix) and other loop diuretics, ethambutol (Myambutol), pyrazinamide, aspirin (low-dose), levodopa (Larodopa), nicotinic acid (Nicolar)
☉Pseudogout	→CPPD: calcium pyrophosphate deposition →knee, large joints, aging-associated