Renal and urinary: USMLE Step 1 video lessons
The kidney from filtration and clearance to acid-base balance, electrolytes and tubular disorders.
Read an arterial blood gas from first principles: normal ranges and the Henderson–Hasselbalch ratio, the anion gap, Winters' formula for expected compensation and the delta ratio. Then how the kidney makes new bicarbonate, the causes of a high anion gap acidosis, the osmolar gap for toxic alcohols, and the urine anion gap for telling diarrhea from renal tubular acidosis.
5:35ABG interpretation, made simple
ABG interpretation from three numbers: pH, PaCO₂ and HCO₃⁻. Learn the normal ranges, the 20 : 1 ratio behind pH, and a three-step method for naming the primary disorder and its compensation.
5:25Anion gap explained: high vs normal gap metabolic acidosis
How to calculate the anion gap, why an added acid widens it while bicarbonate loss does not, and how a low albumin can hide a high-gap acidosis.
5:10Winters' formula: the expected PaCO₂ in metabolic acidosis
Winters' formula tells you how far the PaCO₂ should fall in a metabolic acidosis. Compare the measured value with that window and a hidden respiratory disorder shows itself.
5:09Delta ratio: find the hidden second acid–base disorder
The delta ratio compares the rise in the anion gap with the fall in bicarbonate. In a high anion gap acidosis, it shows whether a second metabolic disorder is hiding.
5:23New bicarbonate: how the kidney excretes acid with ammonium
The kidney reclaims the bicarbonate it filters, but that never makes new bicarbonate. Only excreting acid does, on two urinary buffers: titratable acid and ammonium.
5:54High anion gap metabolic acidosis causes, sorted by the anion
A high anion gap shows that an unmeasured anion has arrived, but not which one. Sort the causes of high anion gap metabolic acidosis by the anion that is actually there.
5:31Osmolar gap: how toxic alcohols hide from the anion gap
The osmolar gap is measured minus calculated osmolality. It picks up uncharged particles such as methanol and ethylene glycol, which raise it early, before the anion gap opens.
5:33Urine anion gap: telling diarrhea from RTA
Two patients can share the same normal anion gap acidosis, one from the gut and one from the kidney. The blood can't tell them apart, but the urine anion gap can.
5:24Renal tubular acidosis: tell RTA types 1, 2 and 4 apart
Renal tubular acidosis gives the same normal anion gap blood picture in three different ways. The mechanism, the urine pH and the serum potassium separate type 1, type 2 and type 4.
5:30Metabolic alkalosis: generation, maintenance and urine chloride
A metabolic alkalosis needs both an event that raises bicarbonate and a kidney that keeps it. Urine chloride shows which kind of maintenance is at work and whether saline will help.
5:36Vomiting metabolic alkalosis: why the urine turns acid
Vomiting removes gastric acid and chloride, leaving a hypochloraemic, hypokalaemic metabolic alkalosis. Yet the urine is acid, a finding called paradoxical aciduria.
5:21Bartter vs Gitelman: NKCC2, NCC and urine calcium
Bartter syndrome behaves like an inherited loop diuretic and Gitelman syndrome like an inherited thiazide. Both cause metabolic alkalosis, but they split on urine calcium.
5:22Respiratory acidosis compensation: acute vs chronic
In respiratory acidosis the lungs are the problem, so compensation comes from buffers first and from the kidney later. Learn the expected HCO₃⁻ for the acute and the chronic phase.
5:33Respiratory alkalosis compensation: acute vs chronic
Two patients can breathe the same way and still have different bicarbonate. Respiratory alkalosis compensation comes in two waves, and the kidneys need days to deliver the second.
5:12Metabolic alkalosis compensation: the expected PaCO₂
In metabolic alkalosis the lungs compensate by breathing less, but only weakly. Use the expected PaCO₂ to tell appropriate compensation from a second respiratory disorder.
5:31Salicylate poisoning acid-base: a classic mixed disorder
Salicylate hits the brain and the mitochondria, so two primary disorders appear together. Use the anion gap and Winters' expected PaCO₂ to recognise the mix.
5:33Type A vs type B lactic acidosis: split it by mechanism
The same lactate can come from a patient in shock or from one with normal perfusion. Ask one question, is perfusion adequate, to separate type A from type B lactic acidosis.
5:42DKA anion gap explained: from high gap to hyperchloraemic acidosis
In diabetic ketoacidosis the anion gap starts high. During treatment it can close while the patient is still acidotic, because ketoanions leave in the urine and chloride takes their place.
5:43Acidosis and hyperkalemia: how pH shifts potassium
Two patients can share the same blood pH and have different potassium. In acidosis and hyperkalemia, the type of acid matters, not just the pH, and the anion gap tells you which acid you have.
5:32ABG interpretation in 6 steps: the acid-base algorithm
One fixed sequence makes ABG interpretation systematic. A normal pH does not clear a gas, and a missed compensation window or a high delta ratio exposes the second disorder.
5:44Acid-base practice cases: three ABG vignettes, one algorithm
The same six steps solve one, two or three acid-base disorders. Work through two ABG vignettes in full, then try the practice case yourself.
How the kidney filters blood: the Starling forces that drive glomerular filtration, how the afferent and efferent arterioles set GFR, renal plasma flow and filtration fraction, and how inulin, creatinine and PAH clearance measure them.
5:25GFR and Starling forces at the glomerulus
Three pressures across the capillary wall set the net filtration pressure, and GFR is Kf times that number. Use them to predict why a kidney stone lowers filtration.
5:16Afferent vs efferent arteriole: GFR, RPF and filtration fraction
Two resistors set the pressure in the glomerulus. Learn the 2×2 table of afferent and efferent constriction and dilation, and use it to explain NSAID and ACE inhibitor kidney injury.
5:20Renal clearance: inulin, creatinine and PAH
Renal clearance is a bookkeeping volume, not a real flow. Use the same equation to estimate GFR with inulin and creatinine, effective renal plasma flow with PAH, and to read what the tubule did.
4:55Glucose transport maximum, splay and SGLT2
Glucosuria is not a leak in a healthy pipe. It appears when the filtered load exceeds a finite carrier capacity, the glucose transport maximum, and splay makes it start earlier than the simple threshold predicts.
5:02Countercurrent multiplier: how the kidney concentrates urine
No pump in the kidney moves water, yet urine can be several times as concentrated as plasma. The countercurrent multiplier, urea recycling and vasa recta build the medullary gradient that ADH lets the duct use.
5:20Aldosterone and ADH in the distal nephron
Two hormones act on the same stretch of tubule but do different jobs. Aldosterone moves sodium in and potassium and hydrogen out; ADH only opens water channels.
5:53Diuretics by nephron segment: loop, thiazide and more
Each diuretic class blocks one transporter in one nephron segment, and that transporter predicts the whole lab pattern. Map the four stops, then split loops from thiazides on calcium.
5:23RAAS explained: renin, angiotensin II and aldosterone
The renin–angiotensin–aldosterone system explained step by step: three triggers for renin release, four jobs for angiotensin II, and what aldosterone does in the collecting duct.