• Urinary Na < 20 mmol/L (holding onto Na)
• Urinary Osm > 400 mOsm/L (holding onto water)
• Hyaline casts
• FeNa < 1% (holding only Na)
• Urea/Creatinine >0.07 mmol/umol (urine flow is lower is less so you can't excrete as much urea, also urea follows water)
• oliguria (flow <20ml/min)

• Oligoanuria: oliguria is <400 ml/day, anuria is <100 ml/day
• Acute Azotemia: rising blood urea and creatinine

• Prerenal: hypoperfusion for any reason (ex; blood loss, dehydration, volume maldistribution in sepsis or liver disease, or low CO due to CHF
• Post-renal: urinary tract obstruction for any reason at any level

1. Insterstitial renal disease

- ATN post ischemia

- Endogenous toxins: (heme from rhabdomyolysis or Hgbemia, light chain disease due to MM, Uric acid following cytotoxic chemo or in lymphoma)

- Exogenous toxins: aminoglycoside Ab, Ethylene glycol (due to it's metabolite oxalic acid and oxalate deposition), radiocontrast material

- Tubular inflamation: drug allergy or infectious

2. Glomerular

- 1 or systemic disease with renal involvement. *most common is any type of RPGN

3. Vascular

- thrombosis or microangiopathic process, intravascular hemolysis or microangio. thrombosis as seen is HUS and TPP which are caused by diarhea due to toxicity, SLE and postpartum/BCP.

• If it is >100 ml/hr then you may suspect a nephrotoxic origin

• They are compounds used for antibiotics (many of the -mycins)
• given to old people who undergo surgery or are immunosupressed and get sepsis

About 70% of people meeding dialysis are ARF and 30% ESRD. 55% recover, 40% die, and 5% survived but never regained renal function.

*So people recover from renal failure! They sometimes need dialysis while their kidney's don't work until they get better!

• Stable phase: low GFR and no tubular function. oliguric or non-oliguric. You have to manage everything with dialysis
• Early recovery phase: increase in GFR and urinary output
• Late recovery phase: GFR is adequate

• patients with evidence of sturctual or functional kidney abnormalities that persist for at least 3 months, with or without decreased GFR (diabetic microalbiminuria as the commonest cause)
• decreased GFR is , 60 ml/min.1.73m2
• BUT everything here will LEAD to a decreased GFR

• GFR more than 90 ml/min
• presence of hematuria, proteinuria or cysts without decline in GFR
• Amber therapeutic zone meaning prevention and renoprotective therapy

• GFR between 60 and 90
• Amber therapy

• GFR between 30 and 60 ml/min
• Amber therapy

• GFR between 15 and 30 ml/min
• Here it is too late to prevent progression and you must manage complications and prepare for renal replacement therapy
• Red therapeutic zone

• GFR less than 15 ml/min
• the adaptice response can no longer compensate for a reduction in renal mass to this level. The uremic toxins accumulate
• Blue therapeutic zone

Glomerular disease

- Diabetic Nephropathy

- Chronic GNs

Non-glomerular disease or Tubular interstitial disease

- Hypertension

- Chronic insterstial nephropathy (reflux or obstruction, pyelonephritis, toxic nephropathy

- Polycystic kidney disease

• Use it for stable CKD patients older than 18 when their GFR<60ml/min without extreme body habitus and not pregnant.
• Takes into account age, gender, serum creatinine and if AfroAmerican.

• loose their abililty to properly alkalinize their urine, the metabolism of glutamine that creates the ability to alkalinize the urine and that process is insulin dependent
• people whose urine is alkaline like type 1 RTA where you more commonly form calciumphosphate stones

• calcium oxalate
• calcium phosphate
• uric acid now getting mor common cause of stones cause of lots of DM

• idiopathic is 90%
• too much Ca (absorptive-from diet, renal leak, resorptive-from bone)
• too much oxalate (ex; you loose Ca in stool from diarrhea and then it won't bind to the oxalate as much, so chrones, colitis, IBS)
• some genetic conditions
• uric acid can be a troublemaker (forms crystals that calcium phosphate grows on top of)

• you can medicate people to increase their urinary citrate
• type 1 RTA can bring down your citrate
• citrate prevents stone formation
• chronic acidosis will loose alkali in stool, and when your urine is acidic you bring down your citrate
• UTI can make it lower

• primary hyperparathyroidisn
• sarcoidosis
• hyper or hypothyroidism
• Addison's disease

• the ones that are not calcium oxalate

• history, physical, x-ray
• follow up
• about half will make another stone after 10 years
• don't look for a problem too early
• take too much vit C? vit D? occupation (can't stop and pee? getting too dehydrated)

• Kidneys ureter bladder x-ray
• most stones will show up on KUB
• it's got a low dose radiation so it's better for follow up
• you should get urinalysis as well and serum chemistry
• always get a KUB when you do a CT

• K, Cl, bicarb, Ca, phosphate, albumin, alkaline phosphatse (bone turnover)

• increase fluid
• decrease salt (the more salt you get the more Ca you loose in your urine)

• happens with DM pts
• radiolucent (visible on CT with contrast only)
• portugese and italian, Ashkanazi Jewish
• caused by persistantly acid urine
• alkalinizing the urine will dissolve them (we do this naturally after we eat cause we get that bllod alkalization thing then we get rid of the alkali in our pee, cool cool). Give K-citrate.

• It would bring them up. This is because SNS action tends to bring K into cells, and it does that through beta receptors
• Dehydration would increase in intracellular K concentration, so then K would follow the water and go into serum
• Acidosis means there's too much H lying around so it exchanges H going into the cell for K coming out, and causes hyperkalemia. However, if the acidosis was very longstanding then it would ultimately increase flow (somehow) and that would cause net excretion of K resulting in hypokalemia.

• in acidosis, the albumin is all tied up with H+, so there is more free Ca2+, acidosis also increases Ca2+ reabsorption in the tubules
• in alkalosis, more albumin is free to bind Ca2+ and so it can cause a hypocalcemia

• They block the K/Na/Cl cotransporter in the tick ascending Loop of Henle
• They decrease the nephrons ability to make the medulla salty, so that it is not possible to use that gradient in the collecting tubules to concentrate the urine
• It makes the urine saltier, so it takes even more water with it when it leaves

• chlorothiazide, hydrochlorothiazide (it has the word thiazide in it!)
• it inhibits Na and Cl resorption in the early distal tubule

• it's a carbonic anhydrase inhibitor
• this will decrease bicarb reasborption in the proximal tubules
• they can cause acidosis (but maybe we want that, like in the mountain climber!)
• It causes us to loose water with the bicarb too (it's a mild diuretic)

• it's an aldosterone inhibitor!
• spirinolactone, eplerenone and triampterine and the others
• they increase tubular Na so it attracts water into the urine
• it increases plasma K+ and H+ by blocking aldosterone action.
• Note: amiloride and triampterene actually block Na channels directly, still cause hyperkalemia

• Hyponatremia: H20 into CNS. So the symptoms of cerebral edema (nausea, encephalopathy and seizures)
• Hypernatremia: H2O out of CNS. So the symptoms of cerebral water loss which includes vessel rupture (cause the fluid goes into the vessels and overwhelms them), lethargy, seizures, coma.

• Give Ca2+!

• Hypokalemia: increase in electrical conduction. Tachicardia, decreased T wave to a U wave, muscle weakness, fatigue, cramping, paralysis, rhabdomylysis.
• Hyperkalemia: decrease in electrical conduction. Cardiac conduction block (2st, 2nd and 3rd degree blocks plus any bradyarrhythmia), GI symptoms (nausea, vomiting, ileus), paralysis when very severe.

• hypokalemia stimulates renin and supresses aldosterone
• hyperkalemia supresses renin, but directly stimulates aldosterone
• Remember aldosterone's role is to get rid of K. So hypoK should suppress aldo and hyper K should stimulate it. It's effects on renin are counterintuitive (explained once that this is sortof an attempt to keep things balanced)

• Angiotensin II! (there's probably some brain receoptors too).
• But here remember that ADH does not trigger thirst I don't think

• stimulates contraction of mesangial cells
• acts of adrenal glomerulosa cells to increase aldosterone
• constricts the efferent arterioles!
• can stimulate the SNS

• facilitates K uptake in renal and peripheral cells
• increases permeability of lumenal membrane of tubule to K
• enhances distal Na reabsorption
• enhances secretion of K and H in late distal tubules