Clinical decision support that reasons like a nephrologist: stage the CKD, localize the AKI, stabilize the potassium, correct the sodium — with the decision rule and exactly what would change it. Built for verified nephrologists.
Two real nephrology questions, each reasoned the way HeyHippocrates answers: the skills fire, the answer is cited, the decision rule is explicit, and what's missing is flagged. Scroll to each.
58-year-old with type-2 diabetes, eGFR 42, urine albumin-to-creatinine ratio 300 mg/g, blood pressure 148/88 — how do I slow progression?
This is CKD G3b with severe albuminuria (A3) — high risk on the KDIGO map. The kidney-protective backbone is a renin-angiotensin blocker (ACE inhibitor or ARB) titrated up, plus an SGLT2 inhibitor, which now slows progression in diabetic and non-diabetic CKD. Target the blood pressure to roughly <130 systolic, optimize glucose, and consider finerenone in diabetic CKD with residual albuminuria.
Decision ruleAlbuminuric CKD → maximize ACEi/ARB + add an SGLT2 inhibitor; BP <130 systolic; glucose control; finerenone for residual albuminuria in diabetic CKD.
Not established from this alone — the potassium, exact eGFR trajectory, volume status and tolerance change the plan.
Potassium 6.8, peaked T waves on the ECG, oliguric AKI — the emergency sequence?
Move in three steps. First stabilize the myocardium with IV calcium (gluconate or chloride) — it protects the heart but does not lower potassium. Then shift potassium into cells with insulin plus glucose and a nebulized beta-agonist. Finally remove it — a loop diuretic if the patient makes urine, a potassium binder, or urgent dialysis for refractory hyperkalemia or the anuric patient. Stop every potassium-raising drug.
Decision ruleHyperkalemia with ECG changes → IV calcium (stabilize) → insulin/glucose + beta-agonist (shift) → diuretic/binder/dialysis (remove); stop K-raising drugs.
Not established from this alone — the ECG, renal function, urine output and the cause change the sequence.
Illustrative simulations. The physician always decides.
The exact questions your field searches for — answered in the format the knowledge base speaks: the answer, the decision rule, what's missing, and the source.
Stage CKD in two dimensions: the eGFR category (G1–G5) and the albuminuria category (A1–A3), which together place the patient on the KDIGO risk map. Slow progression with a renin-angiotensin blocker (especially with albuminuria) and an SGLT2 inhibitor, blood-pressure control to roughly <120–130 systolic, glycemic control, and avoidance of nephrotoxins; finerenone helps in diabetic CKD. Refer by the eGFR and albuminuria thresholds.KDIGO
Decision ruleStage by eGFR (G) + albuminuria (A) on the KDIGO map; ACEi/ARB + SGLT2i, BP control, glucose, avoid nephrotoxins; refer by threshold.
Missing data: the eGFR trend, albuminuria, potassium and blood pressure change the plan.
Stage AKI by the rise in creatinine and the fall in urine output, then localize it: pre-renal (hypovolemia, poor perfusion), intrinsic (acute tubular necrosis, glomerulonephritis, interstitial nephritis) or post-renal (obstruction — get an ultrasound). Optimize volume and perfusion, stop nephrotoxins and review every drug, and treat the cause. Dialyze for a refractory AEIOU indication — acidosis, electrolytes, intoxication, overload or uremia.KDIGO · AKI
Decision ruleStage (creatinine/urine output) → localize (pre/intrinsic/post, ultrasound) → treat the cause + optimize perfusion + stop nephrotoxins; dialyze for AEIOU.
Missing data: the volume status, urine studies, the ultrasound and the timeline drive the diagnosis.
When potassium is high with ECG changes, act in the order stabilize, shift, remove. IV calcium protects the myocardium immediately without lowering potassium; insulin with glucose and a nebulized beta-agonist drive potassium into cells within minutes; then remove it with a loop diuretic, a gut potassium binder, or dialysis for the anuric or refractory patient. Recheck the level and stop the offending drugs.guideline synthesis
Decision ruleECG changes → IV calcium (stabilize) → insulin/glucose + beta-agonist (shift) → diuretic/binder/dialysis (remove); recheck; stop K-raising drugs.
Missing data: the ECG, renal function, urine output and the cause change the urgency and route.
First ask if it is severe or symptomatic and how acute — severe symptomatic hyponatremia gets hypertonic saline promptly. Then confirm it is truly hypotonic (measure osmolality; exclude hyperglycemia and pseudohyponatremia) and assess volume status: hypovolemic, euvolemic (often SIADH) or hypervolemic. Treat the cause, and correct sodium slowly — no more than about 8 mmol/L in 24 hours — to avoid osmotic demyelination.guideline synthesis
Decision ruleSevere/symptomatic → hypertonic saline; confirm hypotonic + volume status (hypo/eu/hyper) → treat cause; correct ≤8 mmol/L/24 h.
Missing data: symptoms and acuity, the osmolality, volume status and urine studies change the plan.
Your whole practice, one specialist brain — grounded in champion-authored, cited knowledge.
A generalist nephrology colleague across CKD, AKI, electrolytes, glomerular disease and dialysis — cited, non-directive, always with the decision rule.
Deep specialist agents for glomerular disease, dialysis, transplant nephrology and onco-nephrology — each its own soul and knowledge base — plus your own uploaded materials.
From the potassium to the biopsy the margin is thin. Only one of these reasons like a nephrology colleague whose every claim you can trace.
The waitlist is a founding cohort. Members shape the nephrology build, get in before anyone else, and lock the founding price for good.
Leave your name and work email. We'll reach out the moment nephrology opens — with your Founding Nephrologist offer.
One email at launch. No spam, ever.
It reasons in the tools you use — the eGFR and albuminuria categories, the KDIGO map and the potassium ladder — and always shows the reasoning, the decision rule and what would change it. The decision always stays your call.
Both. Residents use it to pressure-test a plan and learn the decision rule; attendings use it as a fast, cited second opinion in clinic and on consults. Access is gated to verified physicians.
Glomerular disease, dialysis, transplant nephrology and onco-nephrology each have their own deep specialist agent on the Pro plan, on top of the full nephrology scope on Basic.
No. It is physician-facing clinical decision support — a cited thinking partner. It does not diagnose, does not treat, and gives no patient-facing advice. The decision always stays with you.
Every answer is grounded only in champion-authored, cited nephrology knowledge — traceable, not hallucinated — and always states the decision rule plus what data is missing, instead of a confident guess.
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