Deep Dives
The syndromes, told in full.
Immersive, citation-grounded monographs on the onco-nephrology lesions worth knowing cold — each from the first description through the mechanism, the landmark studies, the current data, and how it's managed today. Every reference is a real, PubMed-verified paper.
The landscape
Each monograph mapped to the kidney-injury signatures it covers; ATN and electrolyte wasting are the most widely shared. Rows and column headers link through to each dive and injury hub.
| Syndrome | ATN | LYTE | TMA | GLOM | FANC | AIN | XTAL | HTN | CIN | PRE | PSEUDO | SIADH |
|---|---|---|---|---|---|---|---|---|---|---|---|---|
| VEGF-inhibitor TMA | VEGF-inhibitor TMA — Acute Tubular Necrosis: not covered | VEGF-inhibitor TMA — Electrolyte Disturbance: not covered | VEGF-inhibitor TMA — Thrombotic Microangiopathy: primary lesion | VEGF-inhibitor TMA — Glomerular Injury / Proteinuria: secondary | VEGF-inhibitor TMA — Fanconi Syndrome: not covered | VEGF-inhibitor TMA — Acute Interstitial Nephritis: not covered | VEGF-inhibitor TMA — Crystal / Obstructive Nephropathy: not covered | VEGF-inhibitor TMA — Hypertension: secondary | VEGF-inhibitor TMA — Chronic Interstitial Nephropathy: not covered | VEGF-inhibitor TMA — Prerenal / Hemodynamic AKI: not covered | VEGF-inhibitor TMA — Pseudo-AKI: not covered | VEGF-inhibitor TMA — SIADH / Hyponatremia: not covered |
| Cisplatin ATN & hypomagnesemia | Cisplatin ATN & hypomagnesemia — Acute Tubular Necrosis: primary lesion | Cisplatin ATN & hypomagnesemia — Electrolyte Disturbance: secondary | Cisplatin ATN & hypomagnesemia — Thrombotic Microangiopathy: not covered | Cisplatin ATN & hypomagnesemia — Glomerular Injury / Proteinuria: not covered | Cisplatin ATN & hypomagnesemia — Fanconi Syndrome: not covered | Cisplatin ATN & hypomagnesemia — Acute Interstitial Nephritis: not covered | Cisplatin ATN & hypomagnesemia — Crystal / Obstructive Nephropathy: not covered | Cisplatin ATN & hypomagnesemia — Hypertension: not covered | Cisplatin ATN & hypomagnesemia — Chronic Interstitial Nephropathy: not covered | Cisplatin ATN & hypomagnesemia — Prerenal / Hemodynamic AKI: not covered | Cisplatin ATN & hypomagnesemia — Pseudo-AKI: not covered | Cisplatin ATN & hypomagnesemia — SIADH / Hyponatremia: not covered |
| EGFR-inhibitor hypomagnesemia | EGFR-inhibitor hypomagnesemia — Acute Tubular Necrosis: not covered | EGFR-inhibitor hypomagnesemia — Electrolyte Disturbance: primary lesion | EGFR-inhibitor hypomagnesemia — Thrombotic Microangiopathy: not covered | EGFR-inhibitor hypomagnesemia — Glomerular Injury / Proteinuria: not covered | EGFR-inhibitor hypomagnesemia — Fanconi Syndrome: not covered | EGFR-inhibitor hypomagnesemia — Acute Interstitial Nephritis: not covered | EGFR-inhibitor hypomagnesemia — Crystal / Obstructive Nephropathy: not covered | EGFR-inhibitor hypomagnesemia — Hypertension: not covered | EGFR-inhibitor hypomagnesemia — Chronic Interstitial Nephropathy: not covered | EGFR-inhibitor hypomagnesemia — Prerenal / Hemodynamic AKI: not covered | EGFR-inhibitor hypomagnesemia — Pseudo-AKI: not covered | EGFR-inhibitor hypomagnesemia — SIADH / Hyponatremia: not covered |
| Ifosfamide Fanconi | Ifosfamide Fanconi — Acute Tubular Necrosis: secondary | Ifosfamide Fanconi — Electrolyte Disturbance: secondary | Ifosfamide Fanconi — Thrombotic Microangiopathy: not covered | Ifosfamide Fanconi — Glomerular Injury / Proteinuria: not covered | Ifosfamide Fanconi — Fanconi Syndrome: primary lesion | Ifosfamide Fanconi — Acute Interstitial Nephritis: not covered | Ifosfamide Fanconi — Crystal / Obstructive Nephropathy: not covered | Ifosfamide Fanconi — Hypertension: not covered | Ifosfamide Fanconi — Chronic Interstitial Nephropathy: not covered | Ifosfamide Fanconi — Prerenal / Hemodynamic AKI: not covered | Ifosfamide Fanconi — Pseudo-AKI: not covered | Ifosfamide Fanconi — SIADH / Hyponatremia: not covered |
| Pemetrexed tubulopathy | Pemetrexed tubulopathy — Acute Tubular Necrosis: secondary | Pemetrexed tubulopathy — Electrolyte Disturbance: secondary | Pemetrexed tubulopathy — Thrombotic Microangiopathy: not covered | Pemetrexed tubulopathy — Glomerular Injury / Proteinuria: not covered | Pemetrexed tubulopathy — Fanconi Syndrome: not covered | Pemetrexed tubulopathy — Acute Interstitial Nephritis: not covered | Pemetrexed tubulopathy — Crystal / Obstructive Nephropathy: not covered | Pemetrexed tubulopathy — Hypertension: not covered | Pemetrexed tubulopathy — Chronic Interstitial Nephropathy: primary lesion | Pemetrexed tubulopathy — Prerenal / Hemodynamic AKI: not covered | Pemetrexed tubulopathy — Pseudo-AKI: not covered | Pemetrexed tubulopathy — SIADH / Hyponatremia: not covered |
| ICI nephritis | ICI nephritis — Acute Tubular Necrosis: secondary | ICI nephritis — Electrolyte Disturbance: not covered | ICI nephritis — Thrombotic Microangiopathy: not covered | ICI nephritis — Glomerular Injury / Proteinuria: not covered | ICI nephritis — Fanconi Syndrome: not covered | ICI nephritis — Acute Interstitial Nephritis: primary lesion | ICI nephritis — Crystal / Obstructive Nephropathy: not covered | ICI nephritis — Hypertension: not covered | ICI nephritis — Chronic Interstitial Nephropathy: not covered | ICI nephritis — Prerenal / Hemodynamic AKI: not covered | ICI nephritis — Pseudo-AKI: not covered | ICI nephritis — SIADH / Hyponatremia: not covered |
| HD-MTX nephropathy | HD-MTX nephropathy — Acute Tubular Necrosis: secondary | HD-MTX nephropathy — Electrolyte Disturbance: not covered | HD-MTX nephropathy — Thrombotic Microangiopathy: not covered | HD-MTX nephropathy — Glomerular Injury / Proteinuria: not covered | HD-MTX nephropathy — Fanconi Syndrome: not covered | HD-MTX nephropathy — Acute Interstitial Nephritis: not covered | HD-MTX nephropathy — Crystal / Obstructive Nephropathy: primary lesion | HD-MTX nephropathy — Hypertension: not covered | HD-MTX nephropathy — Chronic Interstitial Nephropathy: not covered | HD-MTX nephropathy — Prerenal / Hemodynamic AKI: not covered | HD-MTX nephropathy — Pseudo-AKI: not covered | HD-MTX nephropathy — SIADH / Hyponatremia: not covered |
| Cytotoxic TMA | Cytotoxic TMA — Acute Tubular Necrosis: not covered | Cytotoxic TMA — Electrolyte Disturbance: not covered | Cytotoxic TMA — Thrombotic Microangiopathy: primary lesion | Cytotoxic TMA — Glomerular Injury / Proteinuria: not covered | Cytotoxic TMA — Fanconi Syndrome: not covered | Cytotoxic TMA — Acute Interstitial Nephritis: not covered | Cytotoxic TMA — Crystal / Obstructive Nephropathy: not covered | Cytotoxic TMA — Hypertension: not covered | Cytotoxic TMA — Chronic Interstitial Nephropathy: not covered | Cytotoxic TMA — Prerenal / Hemodynamic AKI: not covered | Cytotoxic TMA — Pseudo-AKI: not covered | Cytotoxic TMA — SIADH / Hyponatremia: not covered |
| Tumor lysis | Tumor lysis — Acute Tubular Necrosis: not covered | Tumor lysis — Electrolyte Disturbance: secondary | Tumor lysis — Thrombotic Microangiopathy: not covered | Tumor lysis — Glomerular Injury / Proteinuria: not covered | Tumor lysis — Fanconi Syndrome: not covered | Tumor lysis — Acute Interstitial Nephritis: not covered | Tumor lysis — Crystal / Obstructive Nephropathy: primary lesion | Tumor lysis — Hypertension: not covered | Tumor lysis — Chronic Interstitial Nephropathy: not covered | Tumor lysis — Prerenal / Hemodynamic AKI: not covered | Tumor lysis — Pseudo-AKI: not covered | Tumor lysis — SIADH / Hyponatremia: not covered |
| BRAF/MEK tubular | BRAF/MEK tubular — Acute Tubular Necrosis: primary lesion | BRAF/MEK tubular — Electrolyte Disturbance: secondary | BRAF/MEK tubular — Thrombotic Microangiopathy: not covered | BRAF/MEK tubular — Glomerular Injury / Proteinuria: not covered | BRAF/MEK tubular — Fanconi Syndrome: secondary | BRAF/MEK tubular — Acute Interstitial Nephritis: secondary | BRAF/MEK tubular — Crystal / Obstructive Nephropathy: not covered | BRAF/MEK tubular — Hypertension: not covered | BRAF/MEK tubular — Chronic Interstitial Nephropathy: not covered | BRAF/MEK tubular — Prerenal / Hemodynamic AKI: not covered | BRAF/MEK tubular — Pseudo-AKI: not covered | BRAF/MEK tubular — SIADH / Hyponatremia: not covered |
| Bisphosphonate injury | Bisphosphonate injury — Acute Tubular Necrosis: secondary | Bisphosphonate injury — Electrolyte Disturbance: secondary | Bisphosphonate injury — Thrombotic Microangiopathy: not covered | Bisphosphonate injury — Glomerular Injury / Proteinuria: primary lesion | Bisphosphonate injury — Fanconi Syndrome: not covered | Bisphosphonate injury — Acute Interstitial Nephritis: not covered | Bisphosphonate injury — Crystal / Obstructive Nephropathy: not covered | Bisphosphonate injury — Hypertension: not covered | Bisphosphonate injury — Chronic Interstitial Nephropathy: not covered | Bisphosphonate injury — Prerenal / Hemodynamic AKI: not covered | Bisphosphonate injury — Pseudo-AKI: not covered | Bisphosphonate injury — SIADH / Hyponatremia: not covered |
| CAR-T AKI | CAR-T AKI — Acute Tubular Necrosis: secondary | CAR-T AKI — Electrolyte Disturbance: secondary | CAR-T AKI — Thrombotic Microangiopathy: not covered | CAR-T AKI — Glomerular Injury / Proteinuria: not covered | CAR-T AKI — Fanconi Syndrome: not covered | CAR-T AKI — Acute Interstitial Nephritis: not covered | CAR-T AKI — Crystal / Obstructive Nephropathy: not covered | CAR-T AKI — Hypertension: not covered | CAR-T AKI — Chronic Interstitial Nephropathy: not covered | CAR-T AKI — Prerenal / Hemodynamic AKI: primary lesion | CAR-T AKI — Pseudo-AKI: not covered | CAR-T AKI — SIADH / Hyponatremia: not covered |
| Proteasome-inhibitor TMA | Proteasome-inhibitor TMA — Acute Tubular Necrosis: not covered | Proteasome-inhibitor TMA — Electrolyte Disturbance: not covered | Proteasome-inhibitor TMA — Thrombotic Microangiopathy: primary lesion | Proteasome-inhibitor TMA — Glomerular Injury / Proteinuria: not covered | Proteasome-inhibitor TMA — Fanconi Syndrome: not covered | Proteasome-inhibitor TMA — Acute Interstitial Nephritis: not covered | Proteasome-inhibitor TMA — Crystal / Obstructive Nephropathy: not covered | Proteasome-inhibitor TMA — Hypertension: not covered | Proteasome-inhibitor TMA — Chronic Interstitial Nephropathy: not covered | Proteasome-inhibitor TMA — Prerenal / Hemodynamic AKI: not covered | Proteasome-inhibitor TMA — Pseudo-AKI: not covered | Proteasome-inhibitor TMA — SIADH / Hyponatremia: not covered |
| Pseudo-AKI | Pseudo-AKI — Acute Tubular Necrosis: not covered | Pseudo-AKI — Electrolyte Disturbance: not covered | Pseudo-AKI — Thrombotic Microangiopathy: not covered | Pseudo-AKI — Glomerular Injury / Proteinuria: not covered | Pseudo-AKI — Fanconi Syndrome: not covered | Pseudo-AKI — Acute Interstitial Nephritis: not covered | Pseudo-AKI — Crystal / Obstructive Nephropathy: not covered | Pseudo-AKI — Hypertension: not covered | Pseudo-AKI — Chronic Interstitial Nephropathy: not covered | Pseudo-AKI — Prerenal / Hemodynamic AKI: not covered | Pseudo-AKI — Pseudo-AKI: primary lesion | Pseudo-AKI — SIADH / Hyponatremia: not covered |
| Drug-induced SIADH | Drug-induced SIADH — Acute Tubular Necrosis: not covered | Drug-induced SIADH — Electrolyte Disturbance: not covered | Drug-induced SIADH — Thrombotic Microangiopathy: not covered | Drug-induced SIADH — Glomerular Injury / Proteinuria: not covered | Drug-induced SIADH — Fanconi Syndrome: not covered | Drug-induced SIADH — Acute Interstitial Nephritis: not covered | Drug-induced SIADH — Crystal / Obstructive Nephropathy: not covered | Drug-induced SIADH — Hypertension: not covered | Drug-induced SIADH — Chronic Interstitial Nephropathy: not covered | Drug-induced SIADH — Prerenal / Hemodynamic AKI: not covered | Drug-induced SIADH — Pseudo-AKI: not covered | Drug-induced SIADH — SIADH / Hyponatremia: primary lesion |
Anti-angiogenics & the glomerular endothelium
VEGF-inhibitor thrombotic microangiopathy
Starve a tumor of its blood supply and you also cut the survival signal podocytes whisper to the glomerular endothelium next door — the capillary tuft answers with thrombi, protein spilling into the urine, and a blood pressure that will not come down.
Platinum & the proximal tubule
Cisplatin acute tubular necrosis & hypomagnesemia
The drug that cures testicular cancer poisons its own portal of entry — pumped into the kidney's S3 tubule by OCT2, cisplatin necroses the proximal tubule and, downstream, silences the distal magnesium channel, leaving patients wasting magnesium long after the last dose.
Anti-EGFR antibodies & the distal tubule
EGFR-inhibitor hypomagnesemia
By occupying the EGF receptor that keeps the TRPM6 channel trafficked to the apical membrane of the distal tubule, cetuximab and panitumumab convert the kidney into a magnesium sieve — an on-target, designed-in toxicity that deepens the longer the drug keeps working.
Oxazaphosphorine alkylators & the proximal tubule
Ifosfamide Fanconi syndrome
Mesna guards the bladder, but nothing guards the proximal tubule — ifosfamide's chloroacetaldehyde metabolite is made inside the tubular cell itself, draining its energy and its reabsorptive machinery until phosphate, glucose, bicarbonate, and amino acids leak into the urine.
Antifolates & the slow erosion of the tubule
Pemetrexed tubular nephrotoxicity
Pemetrexed leaves the body through the kidney, so the tubule sees the drug at every cycle — and the injury accumulates quietly, cycle by cycle, into a tubulointerstitial scar that often does not heal once the drug is finally stopped.
Immunotherapy & the loss of renal tolerance
Checkpoint-inhibitor acute interstitial nephritis
Release the brakes on the immune system to fight the cancer and, weeks to months later, the same unleashed T cells can turn on the kidney's interstitium — a delayed, often steroid-responsive nephritis that hides behind a bland urine and a slowly rising creatinine.
An antifolate, an acidic tubule, and enzymatic rescue
High-dose methotrexate crystal nephropathy
High-dose methotrexate is cleared by the kidney, so when it and its poorly-soluble metabolite crystallize in the acidic tubular lumen the kidney injures itself — and because that same kidney is what clears the drug, injury feeds a spiral of rising levels that leucovorin cannot break but an enzyme can.
When the cumulative dose poisons the endothelium
Gemcitabine and mitomycin thrombotic microangiopathy
Two old cytotoxics — mitomycin and gemcitabine — injure the microvascular endothelium directly and in proportion to the cumulative dose, so months into therapy the small vessels clot, red cells shear, platelets fall, and the kidney fails: a dose-dependent thrombotic microangiopathy that is not TTP, does not respond to plasma exchange, and is answered first by stopping the drug.
When the tumor dies faster than the kidney can clear it
Tumor lysis syndrome
Effective therapy can kill a large, fast-dividing cancer so abruptly that the cells spill their contents into the blood — potassium, phosphate, and a flood of purines that becomes uric acid — and the two crystals that result, urate and calcium-phosphate, clog and poison the tubules: a metabolic emergency that is largely preventable with hydration, rasburicase, and, for venetoclax, a deliberately slow dose ramp-up.
A targeted drug that hits the wrong target — in the kidney
BRAF/MEK-inhibitor tubular injury
Vemurafenib was built to block a mutated melanoma kinase, but in the kidney its damage is off-target: it injures the proximal tubule and can produce a Fanconi picture, usually early and usually mild — and, paradoxically, pairing it with a MEK inhibitor makes it gentler on the kidney, not harsher.
One drug class, two very different kidney lesions
Bisphosphonate nephrotoxicity
The intravenous bisphosphonates that protect bone in myeloma and metastatic cancer split the nephron between them — pamidronate poisons the podocyte and produces a collapsing FSGS with nephrotic-range proteinuria, while zoledronate poisons the proximal tubule and produces a toxic ATN — and both are dose- and infusion-rate-dependent, so the same monitoring that catches them also prevents them.
The kidney caught in the cytokine storm
CAR-T cytokine-release acute kidney injury
CAR-T cells cure by inflammation, and the same cytokine-release syndrome that fevers and drops the blood pressure starves the kidney of perfusion — so the acute kidney injury after CAR-T is mostly pre-renal and mostly reversible, yet the patients who develop it are the sicker ones, and they do worse.
Carfilzomib, the endothelium & the complement threshold
Proteasome-inhibitor thrombotic microangiopathy
Weeks into carfilzomib — often with an infection as the second hit — the microvascular endothelium tips into thrombotic microangiopathy: schistocytes and falling platelets, an acute kidney injury the drug set in motion, and an ADAMTS13 that comes back normal because this was never TTP.
Blocked tubular secretion, not injury
Pseudo-AKI: the creatinine rises and the kidney is fine
Creatinine does not only filter — a fifth of it is pushed into the urine by tubular transporters, and a drug that blocks those transporters raises the number without touching the glomerulus, producing a rise that looks like acute kidney injury on every axis except the one that matters.
Retained water, not lost salt
Drug-induced SIADH: the sodium falls and the tumour takes the blame
Hyponatremia is the commonest electrolyte disorder in oncology and its commonest explanation is the cancer itself — which is exactly why a drug that impairs free-water excretion can go on being given for months while the sodium is treated as a feature of the disease.
Medical-education content — not medical advice. Teaching cases are illustrative composites.