Interstitial nephritis natural history, complications and prognosis: Difference between revisions

Revision as of 23:29, 19 July 2018

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [[1]]; Associate Editor(s)-in-Chief:Mohsen Basiri M.D.

Overview

In the majority of patients with TIN, recovery of function has been observed, and improvement immediately occurs upon stopping the offensive agent.

Nevertheless, about 12% of patients may progress to develop ESRD and its complications; and thus require dialysis or transplantation.

Natural History, Complications, and Prognosis

Natural History

The symptoms of (disease name) usually develop in the first/ second/ third decade of life, and start with symptoms such as ___.
The symptoms of (disease name) typically develop ___ years after exposure to ___.
If left untreated, [#]% of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].

Complications

Common complications of TIN include:
- Hypertension
- Electrolyte and acid-base disorders
- ESRD

Prognosis

In the majority of patients with TIN, a full recovery or partial recovery occurs upon stopping the offensive agent. Meanwhileabout 12% of patients may progress to develop ESRD and its complications; and thus require dialysis or transplantation.

it has been suggested previously that the long-term outcome is worse if renal failure lasts for >3 weeks.^[1]^[2]

Two series have shown worse prognosis with increasing age^[3]

Attempts have also been made to gain prognostic information from the renal biopsy. Only the degree of tubular atrophy predicted renal outcome in our series.

Some authors have reported that patchy cellular infiltration predicts a better outcome than diffuse disease^[4] ^[5] However, recent studies have not supported a correlation between the degree of cellular infiltration or tubulitis and outcome^[6] ^[7]. The degree of interstitial fibrosis has been correlated to outcome [29,30], but in other studies there is no such relationship^[8] These conflicting observations may be due to the patchy nature of the disease and the random sampling on renal biopsy. The infiltrate is generally most prominent at the corticomedullary boundary, and the medulla is relatively spared ^[9].

In chronic tubulointerstitial nephritis the most serious long term effect is kidney failure. When the proximal tubule is injured sodium, potassium, bicarbonate, uric acid, and phosphate intake may be reduced or changed, resulting in metabolic acidosis, hypokalemia, hypouricemia, hypophosphatemia. Damage to the distal renal tubule may cause loss of urine concentrating ability and polyuria.

References

↑ Ditlove J, Weidmann P, Bernstein M, Massry SG. Methicillin nephritis. Med Balt 1977; 56: 483–491
↑ Laberke HG, Bohle A. Acute interstitial nephritis: correlations between clinical and morphological findings. Clin Nephrol 1980; 14: 263–273
↑ Kida H, Abe T, Tomosugi N et al. Prediction of the long-term outcome in acute interstitial nephritis. Clin Nephrol 1984; 22: 55–60
↑ Laberke HG, Bohle A. Acute interstitial nephritis: correlations between clinical and morphological findings. Clin Nephrol 1980; 14: 263–273
↑ Kida H, Abe T, Tomosugi N et al. Prediction of the long-term outcome in acute interstitial nephritis. Clin Nephrol 1984; 22: 55–60
↑ Buysen JG, Houthoff HJ, Krediet RT, Arisz L. Acute interstitial nephritis: a clinical and morphological study in 27 patients. Nephrol Dial Transplant 1990; 5: 94–99
↑ Ivanyi B, Hamilton-Dutoit SJ, Hansen HE, Olsen S. Acute tubulointerstitial nephritis: phenotype of infiltrating cells and prognostic impact of tubulitis. Virch Arch 1996; 428: 5–12
↑ Cheng HF, Nolasco F, Cameron JS et al. HLA-DR display by renal tubular epithelium and phenotype of infiltrate in interstitial nephritis Nephrol Dial Transplant 1989; 4: 205–215
↑ Colvin RB, Fang LST. Interstitial Nephritis. In: Tisher CC, Brenner BM, eds, Renal Pathology: With Clinical and Functional Correlations, 2nd Edn, Vol. 1. J. B. Lippincott, Philadelphia, PA, 1994; 723–768

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[1] Ditlove J, Weidmann P, Bernstein M, Massry SG. Methicillin nephritis. Med Balt 1977; 56: 483–491

[2] Laberke HG, Bohle A. Acute interstitial nephritis: correlations between clinical and morphological findings. Clin Nephrol 1980; 14: 263–273

[3] Kida H, Abe T, Tomosugi N et al. Prediction of the long-term outcome in acute interstitial nephritis. Clin Nephrol 1984; 22: 55–60

[4] Laberke HG, Bohle A. Acute interstitial nephritis: correlations between clinical and morphological findings. Clin Nephrol 1980; 14: 263–273

[5] Kida H, Abe T, Tomosugi N et al. Prediction of the long-term outcome in acute interstitial nephritis. Clin Nephrol 1984; 22: 55–60

[6] Buysen JG, Houthoff HJ, Krediet RT, Arisz L. Acute interstitial nephritis: a clinical and morphological study in 27 patients. Nephrol Dial Transplant 1990; 5: 94–99

[7] Ivanyi B, Hamilton-Dutoit SJ, Hansen HE, Olsen S. Acute tubulointerstitial nephritis: phenotype of infiltrating cells and prognostic impact of tubulitis. Virch Arch 1996; 428: 5–12

[8] Cheng HF, Nolasco F, Cameron JS et al. HLA-DR display by renal tubular epithelium and phenotype of infiltrate in interstitial nephritis Nephrol Dial Transplant 1989; 4: 205–215

[9] Colvin RB, Fang LST. Interstitial Nephritis. In: Tisher CC, Brenner BM, eds, Renal Pathology: With Clinical and Functional Correlations, 2nd Edn, Vol. 1. J. B. Lippincott, Philadelphia, PA, 1994; 723–768

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@@ Line 24: / Line 24: @@
 In the majority of patients with TIN, a full recovery or partial recovery occurs  upon stopping the offensive agent. Meanwhileabout 12% of patients may progress to develop ESRD and its complications; and thus require dialysis or transplantation.
-it has been suggested previously that the long-term outcome is worse if renal failure lasts for >3 weeks [10,13];
+it has been suggested previously that the long-term outcome is worse if renal failure lasts for >3 weeks.<ref>Ditlove J, Weidmann P, Bernstein M, Massry SG. Methicillin nephritis. Med Balt  1977; 56: 483–491</ref><ref>Laberke HG, Bohle A. Acute interstitial nephritis: correlations between clinical and morphological findings. Clin Nephrol  1980; 14: 263–273</ref>  <ref></ref>
-Two series have shown worse prognosis with increasing age [10,28],
+Two series have shown worse prognosis with increasing age<ref>Kida H, Abe T, Tomosugi N et al. Prediction of the long-term outcome in acute interstitial nephritis. Clin Nephrol  1984; 22: 55–60</ref>
 Attempts have also been made to gain prognostic information from the renal biopsy. Only the degree of tubular atrophy predicted renal outcome in our series.
-Some authors have reported that patchy cellular infiltration predicts a better outcome than diffuse disease [13,28]. However, recent studies have not supported a correlation between the degree of cellular infiltration or tubulitis and outcome [15,29]. The degree of interstitial fibrosis has been correlated to outcome [29,30], but in other studies there is no such relationship [31]. These conflicting observations may be due to the patchy nature of the disease and the random sampling on renal biopsy. The infiltrate is generally most prominent at the corticomedullary boundary, and the medulla is relatively spared [32].
+Some authors have reported that patchy cellular infiltration predicts a better outcome than diffuse disease<ref>Laberke HG, Bohle A. Acute interstitial nephritis: correlations between clinical and morphological findings. Clin Nephrol  1980; 14: 263–273</ref>  <ref>	Kida H, Abe T, Tomosugi N et al. Prediction of the long-term outcome in acute interstitial nephritis. Clin Nephrol  1984; 22: 55–60</ref> However, recent studies have not supported a correlation between the degree of cellular infiltration or tubulitis and outcome<ref>Buysen JG, Houthoff HJ, Krediet RT, Arisz L. Acute interstitial nephritis: a clinical and morphological study in 27 patients. Nephrol Dial Transplant  1990; 5: 94–99</ref> <ref>	Ivanyi B, Hamilton-Dutoit SJ, Hansen HE, Olsen S. Acute tubulointerstitial nephritis: phenotype of infiltrating cells and prognostic impact of tubulitis. Virch Arch  1996; 428: 5–12</ref>. The degree of interstitial fibrosis has been correlated to outcome <ref></ref> <ref></ref> [29,30], but in other studies there is no such relationship<ref>Cheng HF, Nolasco F, Cameron JS et al. HLA-DR display by renal tubular epithelium and phenotype of infiltrate in interstitial nephritis Nephrol Dial Transplant  1989; 4: 205–215</ref> These conflicting observations may be due to the patchy nature of the disease and the random sampling on renal biopsy. The infiltrate is generally most prominent at the corticomedullary boundary, and the medulla is relatively spared <ref>Colvin RB, Fang LST. Interstitial Nephritis. In: Tisher CC, Brenner BM, eds, Renal Pathology: With Clinical and Functional Correlations, 2nd Edn, Vol. 1. J. B. Lippincott, Philadelphia, PA, 1994; 723–768</ref>.
-In chronic tubulointerstitial nephritis the most serious long term effect is [[kidney failure]].  When the proximal tubule is injured sodium, potassium, bicarbonate, uric acid, and phosphate intake may be reduced or changed, resulting in  [[metabolic acidosis]], [[hypokalemia]], [[hypouricemia]], [[hypophosphatemia]]).  Damage to the distal renal tubule may cause loss of urine concentrating ability and [[polyuria]].
+In chronic tubulointerstitial nephritis the most serious long term effect is [[kidney failure]].  When the proximal tubule is injured sodium, potassium, bicarbonate, uric acid, and phosphate intake may be reduced or changed, resulting in  [[metabolic acidosis]], [[hypokalemia]], [[hypouricemia]], [[hypophosphatemia]].  Damage to the distal renal tubule may cause loss of urine concentrating ability and [[polyuria]].
 ==References==