In Reply: I appreciate the comments of Dr Farag with regard to our publica- tion that chronicled the spectrum of renal lesions encountered in the non- neoplastic kidney of tumor nephrect- omy specimens. 1 Our intent was to heighten pathologists’ awareness of the variety of non-neoplastic lesions of intrinsic and extrinsic origin. We apol- ogize for not citing their study that targeted the renal consequences of the epidemic of obesity and its systemic signature, the metabolic syndrome. 2 Their data on the renal lesions asso- ciated with metabolic syndrome, arter- ial sclerosis with irreversible tubulo- interstitial components, are powerful and especially poignant in view of the modest sample size. They build upon an earlier major contribution from their institution on the non-neoplastic kidney in tumor nephrectomies. 3 The last decade has witnessed tremendous evolution in the treatment of renal malignancies with the expan- sion of nephron-sparing surgical stra- tegies and the emergence of targeted molecular treatments paralleled by recognition by pathologists of their role in affecting the non-oncologic treatment of urologic oncology pa- tients. 4–6 Somewhat ironically, as urol- ogists are moving toward more conservative strategies to conserve the nephron mass, pathologists and clin- icians realize that the non-neoplastic cortex represents an increasingly valu- able clinical and scientific resource. It provides a window to the overall renal status of a patient in cases in which extrapolation from one kidney or a portion of one kidney to the remaining nephron mass is legitimate. 1–3,7 It is the tissue that is used for analysis in selected clinical contexts at a point in the clinical course that would other- wise not represent a legitimate indica- tion for renal biopsy, such as the patients of Alexander et al 2 with the metabolic syndrome. It also contains material to study the molecular soil from which renal malignancies emerge. In recent years, recognition that the preoperative renal baseline in adults with renal neoplasm and its new postoperative set point strongly correlates with risk for chronic kidney disease is solidly entrenched in the uro- logy, nephrology, and pathology lit- erature. 8,9 The predictive value of the selected clinical and staging data has fostered the creation of postoperative nomograms capable of predicting pa- tient-specific survival. 10,11 It may be time to consider the incorporation of findings in the non-neoplastic cortex into these postoperative nomograms. This may increase their predictive power and provide additional incentive to pathologists to consistently report non-neoplastic cortical findings in tumor nephrectomies. The most important patient bene- fit of reporting findings in the non- neoplastic cortex requires a clinician to address modifiable factors that influence a cancer patient’s survival, such as obesity, hypertension, smoking, and dia- betes. Just as a postmortem examination may provide value to the family of the deceased when genetic diseases or life- style issues are identified, which led to the decedent’s condition, the non-neoplastic kidney could influence the same negative lifestyle behaviors of family members, magnifying the benefit of reporting non- neoplastic cortical findings. Admittedly, expectation that iden- tification of the metabolic syndrome or pathologic changes in the non-neoplastic cortex may prolong a patient’s life is a lofty and likely distant goal, as it is predicated on difficult-to-achieve lifestyle modification. This difficult achievement is reflected in the complex definition of metabolism itself, which is “ythe sum of all of the physical and chemical processes by which living organized substance is produced and maintained, and also the transformation by which energy is made available for the uses of the organism.” 12 The wealth of data with regard to a renal cancer patient’s clinical status and pathologic correlates in non-neoplastic kidney allowing survi- val prognostication should induce a medical “climate change.” This change should consist of the expansion of the multidisciplinary urologic oncology treatment team and include in the treatment plans internists and/or ne- phrologists and other professionals in lifestyle modification; otherwise ad- vancements in oncologic therapies will be minimized by the lack of improve- ment in the non-oncologic predispos- ing or coexistent conditions so important to patient survival. Stephen M. Bonsib, MD Department of Pathology, Louisiana State University Health Science Center Shreveport, LA REFERENCES 1. Bonsib SM, Pei Y. The non-neoplastic kidney in tumor nephrectomy specimens: what can it show and what is important? Adv Anat Pathol. 2010;17:235–250. 2. Alexander MP, Patel TV, Farag YM, et al. Kidney pathological changes in metabolic syndrome: a cross-sectional study. Am J Kid Dis. 2009;53:751–759. 3. Bijol V, Mendez GP, Hurwitz S, et al. Evaluation of the nonneoplastic pathology in tumor nephrectomy specimens: predict- ing the risk of progressive renal failure. Am J Surg Pathol. 2006;30:575–584. 4. Schwartz MJ, Kavoussi LR. The evolution of renal surgery for malignancy. J Urol. 2010;184:1251–1252. 5. Rathmell WK, Godley PA. Recent up- dates in renal cell carcinoma. Curr Opin Oncol. 2010;22:250–256. 6. Facchini G, Perri F, Caraglia M, et al. New treatment approaches in renal cell carcino- ma. Anti-Cancer Drugs. 2009;20:893–900. 7. Henriksen KJ, Meehan SM, Chang A. Non-neoplastic renal diseases are often unrecognized in adult tumor nephrectomy specimens: a review of 246 cases. Am J Surg Pathol. 2007;31:1703–1708. 8. Kim HL, Shah SK, Tan W, et al. Estima- tion and prediction of renal function in patients with renal tumor. J Urol. 2009; 181:2451–2561. 9. Weight CJ, Larson BT, Fergany AF, et al. Nephrectomy induced chronic renal insuf- ficiency is associated with increase risk of cardiovascular death and death from any cause in patients with localized cT1b renal masses. J Urol. 2010;183:1317–1323. 10. Raj GV, Thompson RH, Leibovich BC, et al. Preoperative nomogram predicting 12-year probability of metastatic renal cancer. J Urol. 2008;179:2146–2151. 11. Karakiewicz PI, Saurdi N, Capitanio U, et al. Conditional survival predictions after nephrectomy for renal cell carcinoma. J Urol. 2009;182:2607–2612. 12. Dorland’s Medical Dictionary. Philadel- phia: WB Saunders Company. Spontaneous Complete Regression in Merkel Cell Carcinoma After Biopsy To the Editor: We read with interest the author- itative study by Calder and Smoller 1 on new insights into Merkel cell carcino- ma (MCC) which was published in the May issue of the journal. In this study, the authors review the nomenclature, cell origin, clinical presentation, patho- genesis, histopathology, predictors of prognosis, sentinel lymph node bio- psy, and treatment of this tumor. However, a topic that the authors do not mention is the complete spon- taneous regression (CSR) that can be observed in MCC. Despite its high grade of malig- nancy cases of CSR in MCC has been reported. CSR in this tumor is an uncommon and poorly understood phenomenon. A review of the literature Letters to the Editor Adv Anat Pathol  Volume 18, Number 2, March 2011 174 | www.anatomicpathology.com r 2011 Lippincott Williams & Wilkins