To the Editor
The term “congestive kidney” or “congestive nephropathy” has recently been used to describe renal dysfunction associated with venous congestion.1 We encountered a case of proteinuria, which could be related to congestive kidney owing to right heart failure.
A 52-year-old woman with a history of surgery for Tetralogy of Fallot at age 6 years was referred for edema and proteinuria, mainly albuminuria. Imaging results indicated right heart failure and renal congestion owing to repaired Tetralogy of Fallot (Supplementary Figure S1A–D). Her proteinuria persisted despite treatment with diuretics and a renin-angiotensin-aldosterone system inhibitor. She was admitted for a renal biopsy. Laboratory findings are found in Table 1. Serum brain natriuretic peptide levels and urine protein levels (Supplementary Figure S2) revealed a significant positive correlation, suggesting proteinuria can increase when venous congestion worsens.2
Table 1.
Relevant laboratory parameters from referral to admission
| Parameters | At referral | 2 mo after referral | 8 mo after referral | 10 mo after referral | 18 mo after referral | 24 mo after referral | On admission (26 mo after referral) |
|---|---|---|---|---|---|---|---|
| Body weight (kg) | 49 | 47 | 47 | 45 | 46.7 | 45 | 43.6 |
| Cr (mg/dl) | 0.66 | 0.78 | 0.79 | 0.77 | 0.81 | 0.73 | 0.62 |
| eGFR (ml/min per 1.73 m2) | 73.5 | 61.2 | 60 | 61.7 | 58.4 | 65.1 | 77.8 |
| BNP (pg/ml) | ND | 110.4 | 525 | 178.6 | 275.4 | 203.9 | 180.8 |
| Urine protein (g/gCr) | 0.43 | 0.43 | 1.95 | 0.61 | 0.87 | 0.43 | 0.32 |
| Urine NAG (U/gCr) | ND | ND | ND | ND | ND | 13.5 | 11.6 |
| Urine L-FABP (μg/gCr) | ND | ND | ND | ND | ND | 1.5 | 0.8 |
BNP, brain natriuretic peptide; Cr, creatinine; eGFR, estimated glomerular filtration rate; L-FABP, liver-type fatty acid-binding protein; NAG, N-acetyl-β-D-glucosaminidase; ND, not determined.
L-FABP, normal value: ≤8.4 μg/gCr; NAG, normal value: 1.6–5.8 U/gCr.
Renal pathology results revealed normal glomeruli and dilated and atrophic tubules (Figure 1a). The interstitium was slightly edematous, and no interstitial fibrosis was observed (Figure 1b). Notably, peritubular capillaries in the cortex were significantly dilated (>50 μm, normal diameter: 7 μm) (Figure 1c), and vasa recta in the inner medulla were dilated (>30 μm, normal diameter: 7–20 μm) (Figure 1d).3,4
Figure 1.
Representative images of renal biopsy: (a) a normal-sized glomerulus without obvious changes and dilated tubules with no tubulitis or interstitial inflammation (200×, PAS); (b) slight interstitial edema, but no interstitial fibrosis (100×, Masson); (c) significantly dilated peritubular capillaries in the cortex (400×, PAS); and (d) dilated vasa recta in the inner medulla (400×, PAS). PAS, periodic acid–Schiff.
In most animal models of venous congestion, renal function is impaired owing to decreased renal arterial blood flow.1 Notably, in this case, the renal function was relatively normal with slight tubular damage. Despite mildly elevated urinary N-acetyl-β-D-glucosaminidase, urinary liver-type fatty acid-binding protein, the proximal tubular hypoxic marker, was within normal limits. These findings possibly suggest that tubular abnormalities were induced by factors other than renal ischemia. Another notable finding in our case was the dilated peritubular capillaries and vasa recta. In fact, a previous study revealed peritubular capillary dilation in an infrarenal aortocaval fistula-induced congestive heart failure rat model.S1 Therefore, dilated peritubular capillaries and vasa recta can help in the pathologic diagnosis of congestive kidneys at early or less severe stages of renal impairment.
To the best of our knowledge, this is the first renal biopsy case report on congestive kidney. Dilation of peritubular capillaries and vasa recta may be an initial pathologic change in renal congestion.
Ethics Approval and Patient Consent
This study was designed in accordance with the Declaration of Helsinki and approved by the Institutional Review Board of St. Marianna University School of Medicine (Institutional Review Board approval number: 4490). This article does not contain any studies with human participants performed by any of the authors.
Acknowledgments
The authors thank Keiichi Ohata, a researcher of CMIC Holdings Co., Ltd., for scientific advice on urinary liver-type fatty acid-binding protein; Sayuri Shirai, a nephrologist of the Division of Nephrology and Hypertension, Department of Internal Medicine, St. Marianna University School of Medicine, for medical information on urinary N-acetyl-β-D-glucosaminidase; Yasushi Ariizumi, a pathologist of Kawasaki Municipal Tama Hospital, for specimen preparation; and Haruna Ishikawa, a pharmacist at the Kidney Center of Kawasaki Municipal Tama Hospital, for data management in this study. The authors also greatly benefited from the expertise of Editage (www.editage.jp) with regard to English language editing. No funding/grant support has been received for the work described in the submission.
Footnotes
Figure S1. Signs indicating right heart failure and venous congestion: (A) chest radiograph reveals cardiomegaly; (B) contrast-enhanced abdominal computed tomography (CT) imaging reveals dilatation of the inferior vena cava (arrow) and left renal vein; (C) Doppler ultrasonography reveals an interrupted biphasic blood flow of the intrarenal vein; and (D) maintained intrarenal artery flow.
Figure S2. Positive correlation between serum brain natriuretic peptide (BNP) levels and urine protein levels.
Supplementary Reference.
Supplementary Material
Figure S1. Signs indicating right heart failure and venous congestion: (A) chest radiograph reveals cardiomegaly; (B) contrast-enhanced abdominal computed tomography (CT) imaging reveals dilatation of the inferior vena cava (arrow) and left renal vein; (C) Doppler ultrasonography reveals an interrupted biphasic blood flow of the intrarenal vein; and (D) maintained intrarenal artery flow.
Figure S2. Positive correlation between serum brain natriuretic peptide (BNP) levels and urine protein levels.
Supplementary Reference.
References
- 1.Husain-Syed F., Gröne H.J., Assmus B., et al. Congestive nephropathy: a neglected entity? Proposal for diagnostic criteria and future perspectives. ESC Heart Fail. 2021;8:183–203. doi: 10.1002/ehf2.13118. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Mueller A.S., McDonald D.M., Singh H.S., Ginns J.N. Heart failure in adult congenital heart disease: Tetralogy of Fallot. Heart Fail Rev. 2020;25:583–598. doi: 10.1007/s10741-019-09903-0. [DOI] [PubMed] [Google Scholar]
- 3.Apelt K., Bijkerk R., Lebrin F., Rabelink T.J. Imaging the renal microcirculation in cell therapy. Cells. 2021;10:1087. doi: 10.3390/cells10051087. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Zimmerhackl B.L., Robertson C.R., Jamison R.L. The medullary microcirculation. Kidney Int. 1987;31:641–647. doi: 10.1038/ki.1987.46. [DOI] [PubMed] [Google Scholar]
Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.

