November 11, 2026 Update — Severe hypokalemia when losses continue
A new Clinical Mastery review, Correcting Severe Hypokalemia When Losses Continue: Oral Dose Ceilings, Split IR/ER Dosing, and the Evidence Gaps, starts from the variable most repletion plans leave out: the requirement is the deficit plus ongoing losses, and urinary losses can be measured as urine volume × urine K. It sets out what the FDA labels actually say about the 40 mEq per-dose ceiling, why immediate- and extended-release KCl should not be summed toward one ceiling, an evidence analysis of seven repletion practices, the harms of peripheral IV potassium, two illustrative scenarios, and the gaps no study has yet closed. Registered in the Advanced Electrolytes module.
Q7 now distinguishes isolated peaked T waves with a narrow QRS from significant conduction toxicity, and explains the course approach and guideline variation. The case resolution and source teaching were corrected. Urine output, reversible obstruction and appropriate Lokelma use in AKI are now explicit parts of the potassium-removal plan. Q12 replaces the CKD planning graphic with the AKI indications graphic: reassess the need for dialysis daily and sooner with deterioration, without implying benefit from automatic early initiation. The AKI lecture and visual reference carry the same clarification.
A visible teaching block before Case 7 · Q4 explains squamous epithelial cells, mucus threads, mixed bacterial forms, practical collection difficulties and Dr Bland’s “dunker” example. It distinguishes collection clues from proof of contamination and renal tubular cells from squamous cells. Midstream collection does not require stopping the stream.
The same teaching appears in Day 3, the urinalysis interpretation lecture and the visual library, with readable text, downloads and linked evidence. Existing questions and answer keys are retained.
Case 4 now has the modeled HFrEF four-pillar benefit above Q4, kidney-and-heart protection below Q4, iron and hepcidin below Q7, and PTH/vitamin D below Q9. Case 5 shows metformin teaching directly below Q2 and both the macula-densa mechanism and early eGFR-dip teaching below Q6, outside answer reveals.
The Day 2 teaching companion follows the same sequence. Both new graphics are in the visual library and their corresponding non-case lectures. The HFrEF NNT is explicitly a 24-month model; the PTH threshold is labeled individualized faculty practice, with the clinical-outcome evidence gap.
Days 3 and 4 now have a question-to-infographic map and visual explanations with all 127 classroom and self-study questions. Metformin graphics accompany the relevant answers; two new graphics clarify urine findings, delirium and familial hematuria.
Day 3 map · Day 4 map · Metformin question and graphics
Andrew Bland, MD, FACP, FAAP
The question bank now contains 100 original questions mapped to the renal and genitourinary blueprint. All 50 original items were reviewed and revised, with 50 added to close coverage gaps. Five choices, explanations for every option, study review, and a 60-question/60-minute exam block support exam preparation. The classroom case questions remain distinct.
Days 3–5 now include revised clinical decisions, thirteen new teaching graphics, active study links and an explicit Day 5 calcium-capstone timetable. Topics include edema, urine microscopy/FENa, kidney-protective therapy, transplant interactions, ADPKD risk and tolvaptan. Detailed graphics follow the relevant answers.
Day 3 · Day 4 · Day 5 · Follow the edema · ACE inhibitor, ARB, ARNI and GDMT · ADPKD risk and other organs
New and revised graphics carry Andrew Bland, MD, FACP, FAAP. All 31 case pages retain the five navigation buttons.
Additional October 24 teaching: boxed warnings, phenformin/metformin and hormone-trial evidence; stone passage, Flomax, drainage, removal and recent prevention evidence. Studies are linked directly to PubMed.
Cases 4–6 have revised clinical decisions and fourteen new infographics: BP and urine testing, iron and kidney protection, metformin evidence versus labeling, lactic-acidosis safety limits, SGLT2 response, Lokelma, effective kidney perfusion, BUN:creatinine interpretation and oral/IV diuretics. Case 5 includes the FDA menopausal hormone-label example and specialist-directed medication plans. The Day 2 teaching companion keeps the detailed Case 5–6 graphics after the decision. All 31 case pages across Days 1–5 now end with buttons for all days, next case, their teaching day, top of case and website home.
Day 1 now opens with four clear choices: the opening lecture, Case 1, Case 2 and Case 3. Each case opens directly with its integrated teaching and infographics. Days 2–5 use the same simple case menus, and case pages have return-to-day and next-case links. Self-study and supplementary resources remain below the classroom choices.
The Sick Day That Wasn’t Held now focuses on urgent sick-day assessment, ketoacidosis recognition, AKI, fluid reassessment and medication restart planning. Three calculation-heavy acid-base questions were replaced with practical decisions; the potassium-versus-insulin question was removed. Nine questions remain, with matching Day 1 teaching and lecture links.
All 15 self-study and additional cases now match the classroom structure: 110 short lessons before their questions, opening frameworks, lab and treatment infographics, case-specific urgent-threat checkpoints and connected lectures. The material is also collected in each of the five Bring the lecture to the bedside hubs.
Thirty-nine existing visual families are used throughout the cases and remain available in the visual library and their non-case lectures and handouts.
Days 2–5 now match the Day 1 teaching sequence: visual approach before the patient, findings, lab interpretation, then treatment and reassessment. Four collected hubs provide 141 decision primers and the original case/lecture connections: Day 2 Day 3 Day 4 Day 5 .
Teach the new summary-day capstone: a staged integration of electrolytes, CKD, AKI, stones, myeloma and AL amyloid nephrotic syndrome. The seven-lab calcium chart now includes explicit ALP and calcium columns with contextual interpretation. Days 2–5 and all remaining core/self-study cases use a recurring urgent-threat checkpoint. Three new figures are embedded in the visual library and relevant non-case teaching.
Bring the lecture to the bedside — Day 1 now includes a shared treat-urgently framework in the opening lecture and all three cases, hyperkalemia ECG patterns plus treatment timing and potassium-removal guides, the hyponatremia diagnostic swim lanes and treatment guide, AKI evaluation and urine casts, fluid tonicity, and LR versus saline. Teaching covers specimen contamination, Bactrim-related hyperkalemia, adult and pediatric maintenance-fluid evidence, and labeled bag pH. Lecture links are spaced for reading. Each Day 1 case opens with a visual teaching framework and follows approach, findings, lab interpretation, then treatment and reassessment. All 31 figures used in the collection are embedded in relevant standalone lectures and registered in the visual library; the original case placements remain.
Bring the lecture to the bedside — Day 1 collects the complete opening lecture, 32 Learn first sections, seven mechanism figures, six integrated summaries and relevant lecture links. A prominent entry appears under Bring the lecture to the bedside in Cases 1–3 and at the top of Session 1. The original teaching sections, case questions and visual galleries remain available.
Seven Day 1 mechanism infographics and introductory teaching before all 32 Day 1 questions now appear in the linked lectures, the visual library and the case debriefs. They cover potassium redistribution and removal (including Lokelma), serum and urine osmolality, ADH, thiazides, magnesium and SGLT2-associated ketoacidosis.
The Three routes to edema visual now includes a readable fluid-return pathway and a direct link to Edema: The Circulation Cycle Approach. The connection appears in the shared visual-summary hub, the heart-failure and cirrhosis case debriefs, and the downloadable Markdown.
Six new integrated case summaries connect heart–kidney–liver edema, the sick-day cascade, nephrotic complications, sodium disorders, obstruction before and after drainage, and tacrolimus toxicity. The illustrations follow the existing medical-art style and appear in 15 case debriefs. All 31 cases now link to visual review resources; the new summaries include discussion prompts, readable explanations, sources, and related lectures. All six are also in the Visual Reference Library.
The opening lecture’s new SGLT2-versus-loop-diuretic infographic connects each drug’s tubular target to macula-densa sensing, glomerular feedback, and GFR. Discussion questions distinguish an intact sensor from blocked NKCC2 and local feedback from the whole-patient response. The Visual Reference Library entry provides the image, readable explanation, downloads, evidence, and related lectures. The albuminuria section now also documents the published historical A4 precedent and distinguishes its cutoff from this lecture’s teaching threshold.
A new albuminuria infographic connects the filtration barrier, tubular reclamation, and UACR. The interactive heat map now offers standard KDIGO and Bland teaching views. The latter divides A3 into >300–1,000, >1,000–3,000, and “A4” >3,000 mg/g; all remain KDIGO A3, with standard risk colors retained. The library entry includes explanations, category boundaries, sources, and downloads.
The opening lecture’s AKI section now illustrates creatinine rising from 1 to 4 mg/dL while true GFR stays at zero. Worked 2021 CKD-EPI outputs show why routine eGFR can imply residual filtration during nonsteady-state AKI. The new visual-library entry includes the diagram, readable table, sources, zoom, and downloads.
The opening lecture now starts with why we have kidneys, what they regulate, and the RAAS, ADH, EPO, vitamin D, and PTH connections. New discussions link albuminuria with glomerular stress and injury; compare the macula-densa response to SGLT2 inhibitors and loop diuretics; explain charge, tubular uptake, and light-chain injury; and connect these mechanisms into combined clinical disorders. A new creatinine and GFR section connects the blood result with filtration, its limitations, and a guided discussion using the existing interactive glomerular hemodynamics model. The kidney-regulation infographic follows the existing lecture illustration style, with related topic lectures linked beside each function and a guide to all five case sessions. The overview now distinguishes sodium/volume from water/tonicity and includes waste and drug clearance. New RAAS and ADH diagrams connect hormone triggers with kidney effects; ANP and BNP complete the volume-regulation discussion. The skeleton-key image carries a corrected homeostasis message adapted from Joel Topf’s factory-smoke analogy. All four visuals are also available in the Visual Reference Library, with readable explanations, image and Markdown downloads, and links back to the lecture.
The opening lecture now leads the case-based series. Use the blood work, urinalysis, and imaging links for discussion, then explore the AKI–CKD overlap, an interactive GFR–albuminuria heat map, and the limitations of eGFR during rapid creatinine changes. The introduction connects inpatient and outpatient nephrology with the integrated teaching cases.
The Visual Reference Library now uses individually composed medical infographics with integrated anatomical scenes, enlarged mechanisms and topic-specific clinical panels. The rhabdomyolysis abstract shows muscle breakdown, circulating contents and tubular injury as one visual story. The original intrinsic AKI and hyperkalemia compositions are retained. Matching lesson graphics, readable teaching text, evidence links, zoom and full-size PNG downloads are preserved.
The Visual Reference Library has refreshed 325 graphics with light backgrounds, navy serif titles, larger illustrations and precise teaching diagrams. Detailed medical artwork now illustrates the relevant anatomy and mechanisms. The hyperkalemia abstract demonstrates the protect–shift–remove approach in the new style. The original illustrated AKI abstract, full teaching text, source links, zoom and PNG downloads are retained. Matching graphics are updated in the educational pages.
The 326-entry visual reference library now includes 325 redesigned graphics with anatomical schematics, mechanism maps, clinical decision pathways, procedure sequences and labeled charts. The original illustrated AKI abstract is retained. Each updated abstract includes a zoom control, scalable SVG and PNG downloads, a diagram description and the existing full teaching text and source links. Matching graphics are refreshed in the educational pages. Numerical examples are explicitly labeled; diagrams are educational schematics.
The 30-case course now has an eight-stage classroom view with pre-case retrieval, history and examination cards and questions, a lab-order checkbox activity, individual laboratory result cards, post-lab interpretation prompts, clinical decisions and a lecture-linked debrief. Direct lecture links accompany the existing clinical evidence. Full-case view supports study and printing. All 316 scored questions and the original laboratory values and tables are preserved; the new discussions and workup selections are ungraded.
The new Case-Based Lectures section organizes 30 cases into five sessions, with 286 questions, direct answer links, required self-study, a readiness quiz and a lecture-coverage map. The October 12 evidence update adds a source and objective for each question, five additional self-study checkpoints, optional confidence ratings and local first-response CSV export. These are formative teaching cases; faculty and learner validation remain pending. The linked TLS and AKI teaching now distinguishes urgent IV calcium for hyperkalemic ECG changes from avoiding routine calcium for asymptomatic hypocalcemia.
The visual reference library now emphasizes specific findings, decision points, monitoring, and worked examples for each audience. The CKD management visuals show treatment eligibility and follow-up. The urinalysis algorithm uses urine chloride <20 versus ≥20 mEq/L for metabolic alkalosis, with relevant limitations.
Visual reference panels use readable colors in light and dark modes, with one consistent navigation banner per educational collection.
The Visual Reference Library brings together 326 teaching graphics across the public educational collections. Each has a text version, a downloadable image, and links to the full educational material. Matching graphics are embedded in the lecture, student, Primer, Clinical Mastery, patient, and case-report pages.
The AKI BMP guide’s reference links were corrected. Historical ADVOCATE citations are labeled retracted and the associated teaching has been revised. KDIGO 2026 AKI public-review material is identified as draft.
A new Clinical Mastery appraisal of apixaban 2.5 mg twice daily explains why “renally dosed” does not establish effective stroke prevention. It corrects exposure comparisons, distinguishes direct USRDS dose findings from network estimates, and discusses the possibility of bleeding harm without benefit. Includes trial limitations, labeling, and an explicit shared risk–benefit decision. A new comment or correction form is linked at the bottom of every page; the originating page is included automatically.
Linked to the full AF review and N14 nursing card. Maintenance Hemodialysis now has 25 reviews in seven tracks and 23 nursing cards.
A new dialysis section on missed treatments and health-related social needs starts with meeting people where they are: ask why coming is difficult, acknowledge the burden, and make a workable plan together. Includes transportation, work and caregiving, food/housing/utilities, costs, treatment symptoms, communication and support, a barrier-to-action table, and follow-through.
The companion N23 nursing card and two-sided PDF cover the first conversation, safety escalation, and handoff. Maintenance Hemodialysis now has 24 reviews in seven tracks and 23 nursing cards.
Six new focused nursing cards cover lipids, glucose/HbA1c, phosphorus-calcium-PTH, anemia lab review, dialysis adequacy, and preventive screening. Two additional vascular-access cards cover access choices in older adults and fistulas with worsening heart failure, including right-heart failure and HFrEF. The collection now contains 22 HTML cards and 22 two-sided PDFs. Reviews and cards link to one another, with section/home navigation and previous/next links.
The Maintenance Hemodialysis module and nursing-card index now have readable light and dark themes, clearer cards, and consistent theme controls. Plain-text reference addresses in the screening white paper and recently updated reviews now open their sources directly; PubMed links have clearer underlining.
A new Maintenance Hemodialysis module in the Clinical Mastery Series takes the routine decisions of in-center hemodialysis one at a time. Each page covers a single question — which potassium bath, how to set a target weight, how fast to remove fluid, which blood pressure reading to trust — and works through the trials, the guideline positions, and what is still unknown, with PubMed-linked references.
The dialysate prescription (potassium and the rule of 7 versus 8, hyperkalemia, sodium, calcium, buffer, and magnesium); volume and hemodynamics (dry weight, ultrafiltration rate and treatment time, intradialytic hypotension and cooling); blood pressure in dialysis (measurement, treatment, intradialytic hypertension, and a perspective on peridialytic BP as a quality measure); monitoring and preventive care (cardiometabolic risk, CKD-MBD, hepatitis and vaccines, cancer and thyroid screening, adequacy and cognition, and two pages on anemia aligned to KDIGO 2026); nutrition, inflammation, and cardiovascular prevention (protein-energy wasting, the PISCES fish-oil trial, and atrial fibrillation with apixaban on dialysis); and vascular access care (fistula and graft examination and cannulation, catheter care and lock solutions).
Fourteen one-sheet cards for dialysis nurses and technicians. The front lists what to do, when to call the nephrologist, and what not to do; the back gives the reasons, with references. Each prints front and back on one sheet and has a PDF. The physician’s written order and the unit protocol always govern.
The complete screening and health maintenance white paper remains available as a single long read, updated the same day: glycated albumin is now described as an alternative glycemic marker rather than the preferred one, the vaccine table follows the 2026 CDC adult schedule (RSV at 50 or older for patients on dialysis, PCV21, COVID-19 for all adults), and hepatitis C cure rates are stated at about 97%.
IgA nephropathy went from “ACE inhibitor and hope” to nine drug classes in under five years. A new section index organises that landscape by the four-hit model — which agent interrupts which hit, which compartment it actually reaches, and a tiered verdict on what works and on what quality of endpoint.
Toggle any of fourteen agents and three linked panels respond. Panel 1 is B-cell survival and depletion, including the GALT compartment where Gd-IgA1 is actually made. Panel 2 is class-switch recombination, with the T-dependent CD40 route and the T-independent TACI route, and the measured immunoglobulin effects. Panel 3 is the glomerulus, running the same animated hemodynamics simulator used in the creatinine and GFR lecture, extended with the IgA nephropathy agents: select atrasentan, sparsentan, or an ERA plus an SGLT2 inhibitor and the afferent and efferent arterioles, glomerular pressure, GFR and albumin handling all respond, with the NSAID and triple-whammy states kept for contrast.
Three agents with real, measurable B-cell activity fail or only partly succeed here, each for a structurally different reason. Rituximab depletes circulating CD20+ cells completely and reaches neither the GALT source nor the plasma cell, which has shed CD20 — in the randomized trial, Gd-IgA1 and its autoantibodies did not change at all. Mycophenolate blocks lymphocytes that are dividing, and the long-lived plasma cell is post-mitotic. Abatacept removes T-cell help, but mucosal IgA switching runs through a T-independent route that needs no T cell.
Nefecon is the control experiment: it is also a B-cell-killing drug — budesonide is a glucocorticoid — and it works because it is delivered where those cells actually are. Same target, opposite outcome, on compartment access alone.
Two drugs reached the US market within eight months of each other — VOYXACT (sibeprenlimab) in November 2025 and TRUTAKNA (atacicept) in July 2026, the first dual BAFF/APRIL agent. Both are promoted as acting “furthest upstream.” This review asks what the mechanism actually supports.
These agents are often described as targeting galactose-deficient IgA1. They do not. The selectivity is by isotype, not glycoform — and the sibeprenlimab label settles it: at week 48, Gd-IgA1 fell 67% while total IgA fell 69%. They move in lockstep. Nothing reads the hinge-region O-glycan; the pathogenic species declines because the isotype does.
Sibeprenlimab removed 95.8% of circulating APRIL and achieved 67.1% Gd-IgA1 reduction. Atacicept lands at 66–68% across two independent readouts. Three agents, two mechanisms, four timepoints, and the answer keeps converging near two-thirds — evidence of an APRIL-independent reservoir, most likely the IL-6 limb of TLR9 signalling, which no approved agent touches.
The ORIGIN 3 baseline was a geometric mean UPCR of 1.5 g/g. A 46% reduction lands near 0.8 g/g — above the KDIGO 2025 target of <0.5 g/d, ideally <0.3, and inside a band carrying hazard ratios of 1.7 to 4.0 for progression. Worth noting before citing the guideline in support: KDIGO 2025’s list of therapies that reduce pathogenic IgA production does not include any BAFF or APRIL agent. Both approvals postdate it.
Rituximab has been tested in IgA nephropathy in a randomized trial, and the result is one of the most instructive negatives in glomerular disease: it depleted B cells completely, and serum galactose-deficient IgA1 and its autoantibodies did not change. Proteinuria and eGFR were unmoved. The review adds a section on why — the pathogenic IgA1 is made in gut-associated lymphoid tissue, where a depleting antibody penetrates poorly, and the plasma cell that actually secretes it has shed CD20 and is invisible to anti-CD20 everywhere at once. Obinutuzumab, a type II anti-CD20 with deeper tissue depletion, addresses the first problem and cannot address the second; the IgAN evidence for it is a three-patient uncontrolled series. The 2025 KDIGO Controversies Conference reached the same conclusion.
Memory B cells are the only mature B2 subset whose survival is BAFF/APRIL-independent, which predicts relapse on withdrawal and indefinite therapy. TACI drives T-independent responses to bacterial polysaccharides, so polysaccharide vaccines are the specifically impaired class — prefer a conjugate pneumococcal vaccine, and vaccinate before starting. The APRIL-SLE trial measured this directly: pneumococcal titres fell 30% and protective status was lost three times as often as on placebo.
The review also works through the SLE safety precedent in detail, including the finding that both fatal infections in APRIL-SLE occurred with normal IgG — so immunoglobulin monitoring detects one failure mode and is blind to the other. All claims are PMID-anchored.
Three physician-level reviews covering the part of the heart failure story that sits between “symptomatic” and “end-stage” — the part where nephrology usually sees the patient first.
Advanced Heart Failure: Classification, Staging, and Referral Criteria lays out the seven INTERMACS patient profiles with their time frames and the TCS/A/FF modifiers, the HFA-ESC four criteria, and the HFSA and ACCF/AHA referral triggers. It also tracks down the number most often half-remembered: the advanced heart failure criterion of a daily furosemide-equivalent dose above 160 mg or the addition of metolazone — and the 1,354-patient cohort behind it, where survival fell from 83% in the lowest diuretic quartile to 53% above 160 mg/day, with an adjusted hazard ratio of 4.0.
Stage C2D Heart Failure reviews the June 2026 JACC: Heart Failure position statement, which for the first time gives operational criteria for the ambulatory population between stage C and stage D: three required core features, a mapping onto INTERMACS profiles 4 to 7, and eleven supportive features of which four are renal. The review keeps the statement’s own caution — the criteria are proposed, not validated — and notes that the paper scopes itself to HFrEF while 57.7% of advanced heart failure has a mid-range or preserved ejection fraction with identical survival.
Advanced Heart Failure: Therapeutics and Evidence works through the evidence once a patient has left stage C: why guideline-directed therapy does not automatically extend, the C2D adaptation algorithm for hemodynamic and renal ceilings, decongestion including ADVOR and CARRESS-HF, what ESCAPE does and does not say about right heart catheterization, durable mechanical support, and concurrent palliative care. Absolute risk reductions and numbers needed to treat are given alongside hazard ratios throughout, and trial funding is named.
The AI for Clinicians presentation for ACOFP Upper Midwest Clinical Essentials on September 20 is available as a 66-slide PDF. The opening slide includes QR codes to save Dr. Bland's contact card and download the presentation.
Two additions, both built from guidelines read end to end rather than from summaries — which turned out to matter, because two widely repeated numbers did not survive the reading.
A blood pressure number means nothing on its own in a child. The same 118/76 is unremarkable in a tall 16-year-old and frankly hypertensive in a small 4-year-old. The new lecture works through why the reference tables are indexed to sex, age and height — and why not to weight.
The physiology is hydrostatic: every centimetre the brain sits above the heart costs about 0.78 mmHg of perfusion pressure, so a taller organism must generate a higher pressure at heart level. The giraffe settles the argument — roughly 300/200 mmHg at the heart to deliver about 100 mmHg at a brain two metres up, the same cerebral perfusion pressure a human enjoys. It is not hypertensive; it has exactly the pressure its anatomy demands.
Working the AAP tables themselves shows how far that explanation actually reaches. Systolic pressure rises about 0.32 mmHg per cm of height, diastolic only 0.17. A hydrostatic column is a uniform offset, so if it explained everything those two slopes would match — and in early childhood they nearly do, before decoupling through puberty. Hydrostatics accounts for essentially all of the diastolic gradient and roughly two-thirds of the systolic; the remainder is maturation, which also tracks height. And the reason norms are not indexed to weight is sharper still: obesity is the disease, not the yardstick. Index to weight and a heavier child earns a higher “normal” threshold precisely because of the adiposity driving the pressure up.
Two details in the calculator are easy to get wrong by hand. Each table row is anchored at the midpoint of the year — “Age 3” means 3.5 years — and ages 1 to 2 are indexed to recumbent length while ages 3 and up use standing stature. Measure a two-year-old standing, read it against a length-based row, and the height percentile lands in the wrong column.
Four pages covering cardiovascular-kidney-metabolic syndrome, aimed at the reader who keeps being handed a staging system built for a cardiovascular question and asked to answer a kidney one with it.
The staging page states two structural weaknesses plainly, because both bite hardest in nephrology. HbA1c is a switch rather than a dial — 6.5% and 13% both assign stage 2, so severity never escalates the stage. And severe albuminuria with a preserved eGFR sits at stage 2 alongside uncomplicated hypertension, because the framework collapses KDIGO’s four risk bands into two stages. Neither is an oversight by a panel that lacked kidney expertise: ASN was represented, and the guideline cites KDIGO 39 times. Both severities re-enter through the PREVENT add-on models, which take UACR and HbA1c as continuous inputs. That answer is complete for cardiovascular risk and silent on kidney trajectory — KFRE is not validated above an eGFR of 60, so for the young patient with heavy proteinuria and a normal creatinine, neither instrument sees them.
Reading the primary sources rather than summarizing them caught two errors that had been sitting in the underlying reviews.
The stage 2 triglyceride threshold was recorded as 135 mg/dL. That figure appears nowhere in the guideline, which defines hypertriglyceridemia as a fasting triglyceride of 150 mg/dL or a nonfasting 175 mg/dL. Small in magnitude, consequential in kind — it sits directly on the stage 1 / stage 2 boundary, so it moves patients between stages. Corrected, along with a second file the wrong figure had propagated into.
The pre-HF biomarker cut points in wide circulation — NT-proBNP 125, hs-troponin T 14 and 22, hs-troponin I 10 and 12 — return zero matches across the entire guideline. Its pre-HF criterion is qualitative, not numeric. The only biomarker values in the document belong to individual studies: BNP 50 was the STOP-HF screening threshold, and NT-proBNP 40 an entry criterion in a 46-patient exercise trial. Neither is a guideline cut point. Those numbers were removed from these pages rather than published with a caveat, and what the guideline actually supplies — a PREVENT-HF risk trigger for ordering the test, not a threshold for interpreting it — is stated in their place.
A new physician-level Clinical Mastery review covering three drug families that reach the hypertension and kidney clinic constantly and are rarely considered together: antidepressants, anxiolytics, and ADHD medications. The organizing idea is that blood-pressure effect tracks norepinephrine transporter blockade rather than the marketing category — which is why “non-stimulant” ADHD agents are not blood-pressure safe, and why guanfacine lowers adult systolic pressure by roughly 10 mmHg.
Practical content includes the antihypertensive interactions worth avoiding outright (paroxetine and fluoxetine raise metoprolol exposure three- to five-fold; diltiazem raises buspirone exposure 5.5-fold), bupropion’s metabolite trap in dialysis where the parent drug looks reassuringly normal, serotonin syndrome with the Hunter criteria and its rhabdomyolysis consequence, and renal dosing tables for both drug families. The review states plainly where the evidence is thin — there are no ADHD pharmacotherapy studies in CKD populations, and the randomized antidepressant trials in CKD are negative or modest.
The material ships at three depths, so the same evidence reaches a student revising for an exam, a classroom, and a clinician making a prescribing decision:
Four new interactive cases bring the case library from 30 to 34. Each is built around a decision point where the intuitive answer is the wrong one, and each is cross-linked from all three pages above:
A full audit compared every clinical section of this site against the source material behind it. The finding was not that content was missing. It was that a great deal of finished work had never become reachable — written, and then left where no reader could get to it. Today closed most of that gap.
A new lecture, Acute Interstitial Nephritis, joins the AKI module with the complete etiologic taxonomy — every implicated drug class with its characteristic latency, infectious and systemic causes, malignancy, and the genetic tubulointerstitial diseases — and sorts treatment by etiology, with an explicit “do NOT” column for each. It introduces a provenance convention: each substantive claim is tagged EVIDENCE-BASED (anchored to a named study with a PMID) or PRACTICE-BASED (standard teaching, not trial-anchored). AIN has very little randomized evidence, and blurring that line does readers no favors. A companion physician-level review, AIN: Complete Etiology and Etiology-Directed Treatment, carries the same tagging across 31 references.
The correction. Building it surfaced an error on an existing page: the positive likelihood ratio for urine eosinophils was given as 1.83. Checked against the source (Muriithi, CJASN 2013), the correct value is 0.97, and the negative likelihood ratio is 1.01. Both sit at 1.0 — the test moves post-test probability essentially nowhere in either direction. Specificity was corrected from 85% to 68.2%, and “when present, highly suggestive” was removed, since the positive predictive value is 15.6% and most positives are false. Seven pages in total carried some version of the old claim, including two Primer chapters and two handouts; all seven now agree. The bottom line is unchanged but now correctly supported: do not order urine eosinophils.
The Case Report Library — eight long-form teaching cases, roughly 46,000 words — had no inbound link from any page on this site. It is now on the homepage. Two Clinical Mastery modules were missing from the catalog entirely: Advanced Electrolytes, the largest module in the series, and Paraprotein-Related Kidney Disease. Edema & Diuretic Therapy had been unreachable since March. The Mercy Family Practice Residency CKD series is now linked from the case index.
Thirty-two finished handouts are published for the first time, each with a downloadable PDF. Most were written back in February and then sat unpublished because the build that generates handout pages read one vault folder and they had been filed in another. New material spans AKI (staging, ATN, BMP pattern recognition), electrolytes and acid-base (RTA, integrated calcium physiology, phosphorus), glomerular disease (ANCA vasculitis, membranous nephropathy, post-infectious GN, and diagnostic algorithms for glomerular disease and RPGN), CKD (staging, CKD-MBD, anemia, management pathways), dialysis (CRRT, peritoneal dialysis, initiation, vascular access, kinetics and adequacy), pharmacology (drug dosing in CKD, SGLT2 inhibitors), foundations (the BMP and urinalysis master algorithms), and transplant, edema, hypertension, and onconephrology.
Twelve physician-level reviews moved from draft to published. Hypertension gains the newest drug classes — baxdrostat and lorundrostat, the two aldosterone synthase inhibitors, plus aprocitentan, a genuinely new mechanism for resistant hypertension — and acute renal infarction, a diagnosis routinely mistaken for renal colic. Dialysis gains CRRT principles, partial (incremental) PD, and screening and health maintenance on maintenance hemodialysis. CKD gains albuminuria versus proteinuria measurement and phosphate management in ESRD. Also renal amyloidosis beyond AL, platinum nephrotoxicity, and non-dilated obstructive uropathy.
The published statistics had drifted badly — the Clinical Mastery total appeared three separate times on the homepage as 124, 79, and 46. Every count on this page and the homepage has been recomputed from the actual files. The site now holds 481 pages: 121 Clinical Mastery reviews across 21 modules, 118 student reference documents with 107 downloadable PDFs across 21 topics, 30 interactive cases, 17 patient handouts, a 28-chapter Primer, and 11 podcasts.
Open Clinical Mastery → · Browse Student Handouts → · Open the Case Report Library →
The Dialysis Advanced Module now includes two home-therapy resources: Home Hemodialysis with NxStage, a 53-reference clinical white paper covering prescription design, flow fraction, dialysate selection, monitoring, vascular access, and evidence-based assessment; and Home Dialysis Tools and Resources, a curated guide to public HHD and PD tools. Facility standing orders, internal FMC algorithms, and individual staff contact information remain private and were not published.
Open the Dialysis Advanced Module →
Two new physician-level reviews joined the Clinical Mastery Series: Hypertensive Nephropathy (in Hypertension Advanced, cross-listed under CKD Advanced — the topic spans both) and a new Stone Disease topic launching with The Metabolic Stone Workup & the Evidence Behind Stone Prevention — 24-hour urine interpretation, risk-factor–directed therapy, and a critical appraisal of the prevention evidence.
Open the Clinical Mastery Series →
The new patient-facing section of plain-language kidney-health guides grew from 1 to 17 handouts, adapted from Dr. Bland’s own teaching materials into everyday language for patients and families. They are grouped into six areas: understanding kidney disease, medications, food and lifestyle, tests, dialysis, and stones/infections.
| Group | Handouts |
|---|---|
| Understanding Kidney Disease | What Is CKD? · Diabetes and Your Kidneys · CKD Complications · IgA Nephropathy |
| Medications and Your Kidneys | GLP-1 Medicines · SGLT2 Inhibitors · ACE Inhibitors & ARBs · Water Pills (Diuretics) · NSAIDs and Your Kidneys |
| Food, Diet & Lifestyle | Eating Well with Kidney Disease · Potassium · Phosphorus · Home Blood Pressure |
| Tests, Dialysis, Stones | Kidney Biopsy · Understanding Dialysis · Kidney Stones · Preventing UTIs |
A new audience-scoped track for Clarke University Doctor of Physical Therapy students. The DPT curriculum is a bolt-on to the main PA/rotator curriculum — focused on the cardiorenal and nephrology knowledge that PTs need at the bedside and in cardiac rehab, without medication decisions that stay with the prescribing team.
| Component | What's there |
|---|---|
| DPT Landing | curriculum-udpt-pt.html — audience-scoped entry point with cross-links to lectures, handouts, cases. |
| Full PT Lectures (5) | Hydration · High-Salt Foods · Protein for the CKD Patient · Creatine & Kidney Function · NSAIDs & Pain Management. Each with learning objectives, case vignettes, MCQs, and PubMed-cited references. |
| PT Student Handouts (6) | Hydration · High-Salt Foods · Protein · Creatine · NSAIDs/Pain · GLP-1 Receptor Agonists (sarcopenia, peri-op holds, exercise Rx). |
| PT Interactive Cases (5) | Beta-blockers in HFrEF cardiac rehab · SGLT2i + peri-op DKA · Diuretics & triple-whammy AKI · ACEi/ARB/ARNI transitions & angioedema · RAAS + diuretics + heat/orthostasis. All with MCQ + click-for-explanation. |
Five new PT-focused cardiorenal cases added to the interactive case library, all following the enhanced MCQ + click-for-answer pattern with integrated learning points and module cross-links.
Three new curriculum entry points replace the single all-in-one curriculum page for the three main audiences:
Pagefind-powered full-site search is now on every landing page — indexed at deploy time, theme-aware (light/dark), with blue underlined result links. Type any term in the search box at the top of any curriculum page.
76 comprehensive reference handouts across 18 nephrology topics, designed for PA students, medical students, and residents. Each handout features a polished article layout with sidebar table of contents, dark/light mode, and downloadable PDF.
The AKI module grew from 3 pages to 14 deep-dive reviews, now organized into four thematic sections incorporating the KDIGO 2026 AKI/AKD Guidelines.
| Section | New Content |
|---|---|
| Evaluation | AIN & GN Diagnostic Methodologies |
| Etiology | Pre-renal AKI (Cardiorenal/Hepatorenal Syndromes) |
| Etiology | Acute Tubular Necrosis: Intrinsic & Extrinsic |
| Etiology | Obstructive Nephropathy & Imaging |
| Etiology | Retroperitoneal Fibrosis & IgG4-Related Disease |
| Drug-Induced | Drug-Induced AKI Overview & Framework |
| Drug-Induced | Antibiotic-Associated Kidney Injury (12,600 words) |
| Drug-Induced | PPI Nephrotoxicity & AIN |
| Management | KRT Timing & Modality (STARRT-AKI, ELAIN, AKIKI) |
| Management | Loop Diuretics & Furosemide Stress Test |
43 new deep-dive clinical reviews added across 7 mastery sections, drawn from the clinical vault and curated for educational quality (3,000+ word threshold).
| Section | New Pages | Highlights |
|---|---|---|
| Onconephrology | +7 | ICI treatment (MD Anderson), CAR-T kidney, TLS, VEGF/TKI toxicity |
| Electrolytes | +9 | RTA comprehensive (9.3K), metabolic alkalosis (7.9K), ICH hyponatremia |
| Cardiorenal | +6 | Comprehensive report (10.9K), HFpEF roundtable, SGLT2i in T1DM |
| Glomerular | +5 | Lupus nephritis treatment (12.3K), MGUS vs MM scoring (12K) |
| Edema | +3 | Sequential nephron blockade (13.5K), medications causing edema |
| Dialysis | +3 | Enterococcal endocarditis on HD, CCHT exam module |
| CKD | +1 | CKD-MBD comprehensive review |