September 13, 2026 Update — AI for Clinicians conference presentation
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 verified 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 |