graph LR
Decreased_GFR["Decreased GFR"]
RAAS_Activation["RAAS Activation"]
Fatigue["Fatigue"]
Kidney_Transplantation["Kidney Transplantation"]
Hypertension["Hypertension"]
Blood_Pressure_Control["Blood Pressure Control"]
Proteinuria["Proteinuria"]
Peripheral_Edema["Peripheral Edema"]
Glomerulosclerosis["Glomerulosclerosis"]
Dialysis["Dialysis"]
Dietary_Protein_Restriction["Dietary Protein Restriction"]
IL_11_Signalling_in_Renal_Fibroblasts["IL-11 Signalling in Renal Fibroblasts"]
Anemia["Anemia"]
Metabolic_Acidosis["Metabolic Acidosis"]
ACE_Inhibitors_ARBs["ACE Inhibitors/ARBs"]
NMR_metabolomic_risk_score_MetRS["NMR metabolomic risk score (MetRS)"]
Klotho_Deficiency["Klotho Deficiency"]
Creatinine["Creatinine"]
Nephron_Loss["Nephron Loss"]
SGLT2_Inhibitors["SGLT2 Inhibitors"]
AAV_Mediated_Klotho_Gene_Therapy["AAV-Mediated Klotho Gene Therapy"]
Tubulointerstitial_Fibrosis["Tubulointerstitial Fibrosis"]
Nephron_Loss --> Decreased_GFR
Nephron_Loss --> Metabolic_Acidosis
Nephron_Loss --> Glomerulosclerosis
Glomerulosclerosis --> Proteinuria
Glomerulosclerosis --> Nephron_Loss
Klotho_Deficiency --> Tubulointerstitial_Fibrosis
Klotho_Deficiency --> IL_11_Signalling_in_Renal_Fibroblasts
IL_11_Signalling_in_Renal_Fibroblasts --> Tubulointerstitial_Fibrosis
Tubulointerstitial_Fibrosis --> Anemia
Tubulointerstitial_Fibrosis --> Nephron_Loss
RAAS_Activation --> Hypertension
RAAS_Activation --> Peripheral_Edema
RAAS_Activation --> Tubulointerstitial_Fibrosis
Anemia --> Fatigue
ACE_Inhibitors_ARBs --> RAAS_Activation
SGLT2_Inhibitors --> Tubulointerstitial_Fibrosis
Blood_Pressure_Control --> Glomerulosclerosis
Dietary_Protein_Restriction --> Glomerulosclerosis
Dialysis --> Nephron_Loss
Kidney_Transplantation --> Nephron_Loss
AAV_Mediated_Klotho_Gene_Therapy --> Klotho_Deficiency
Nephron_Loss -.-> Creatinine
Nephron_Loss -.-> NMR_metabolomic_risk_score_MetRS
style Decreased_GFR fill:#fef3c7
style RAAS_Activation fill:#dbeafe
style Fatigue fill:#fef3c7
style Kidney_Transplantation fill:#fce7f3
style Hypertension fill:#dcfce7
style Blood_Pressure_Control fill:#fce7f3
style Proteinuria fill:#fef3c7
style Peripheral_Edema fill:#fef3c7
style Glomerulosclerosis fill:#dbeafe
style Dialysis fill:#fce7f3
style Dietary_Protein_Restriction fill:#fce7f3
style IL_11_Signalling_in_Renal_Fibroblasts fill:#dbeafe
style Anemia fill:#fef3c7
style Metabolic_Acidosis fill:#fef3c7
style ACE_Inhibitors_ARBs fill:#fce7f3
style NMR_metabolomic_risk_score_MetRS fill:#e0e7ff
style Klotho_Deficiency fill:#dbeafe
style Creatinine fill:#e0e7ff
style Nephron_Loss fill:#dbeafe
style SGLT2_Inhibitors fill:#fce7f3
style AAV_Mediated_Klotho_Gene_Therapy fill:#fce7f3
style Tubulointerstitial_Fibrosis fill:#dbeafe
name: com_Chronic_Kidney_Disease__Dieulafoy_Lesion
creation_date: "2026-08-16T00:00:00Z"
curation_status: CANDIDATE
notes: >-
Split out of `kb/disorders/Dieulafoy_Lesion.yaml`'s `environmental:` block
(dismech#8302, one of the four "environmental block asserts something the
pathophysiology block cannot receive" instances tracked there): chronic
kidney disease was listed as an "exposure" with no route to either of the
entry's two pathophysiology nodes (both describe the congenital vascular
anomaly itself, not its acquisition or triggering). It is a
comorbidity/host-attribute state, the same category error #8185 tracks, and
is a first-class `Disease` entry in its own right
(`kb/disorders/Chronic_Kidney_Disease.yaml`).
Directionality is UNKNOWN rather than A_BEFORE_B/RISK: the only source is a
within-case comorbidity proportion from a 101-case systematic review of
rectal Dieulafoy lesion (mean age 66±17), with no comparison population.
That is consistent with CKD simply reflecting the age/comorbidity profile
of patients who present with GI bleeding, and the source itself proposes no
mechanism connecting CKD to submucosal-artery caliber persistence or
mucosal erosion. Uremic platelet dysfunction is a plausible route to
*bleeding severity/presentation* rather than to lesion *formation*, but that
distinction is not addressed by this source, so no mechanistic hypothesis is
recorded here. Recording an inferred `RISK` direction would assert more
than the evidence supports (per the dismech#8195 review precedent on
over-claiming from within-case prevalence).
disease_a:
slug: Chronic_Kidney_Disease
preferred_term: chronic kidney disease
term:
id: MONDO:0005300
label: chronic kidney disease
disease_b:
slug: Dieulafoy_Lesion
preferred_term: Dieulafoy lesion
term:
id: MONDO:0001427
label: Dieulafoy lesion
directionality: UNKNOWN
effect_direction: UNKNOWN
association_signals:
- source: LITERATURE
method: LITERATURE_ASSOCIATION
population: >-
Systematic review of 101 published adult rectal Dieulafoy's lesion cases
(MEDLINE, Cochrane, Embase, Scopus), mean age at presentation 66±17
years; within-case comorbidity proportion, no comparison/control
population.
directionality: UNKNOWN
statistics:
metrics:
- metric_type: PREVALENCE
metric_value: 0.16
notes: >-
Proportion of the 101-case rectal Dieulafoy lesion series reporting
chronic kidney disease as a major underlying disorder. Unadjusted for
age and with no comparison population, so this corroborates
co-occurrence in an elderly bleeding-presentation cohort rather than
establishing an elevated risk relative to the general population.
evidence:
- reference: PMID:35243119
reference_title: "Rectal Dieulafoy's lesion: a comprehensive review of patient characteristics, presentation patterns, diagnosis, management, and clinical outcomes."
supports: SUPPORT
evidence_source: HUMAN_CLINICAL
snippet: "Major underlying disorders were hypertension 29%, diabetes mellitus 21%, and chronic kidney disease 16%."
explanation: >-
Reports chronic kidney disease as an underlying comorbidity among a
systematic review cohort of rectal Dieulafoy lesion cases.