Hypertrophy of the Kidney (part 2) With Pictures!
In a 2009 study, compensatory renal enlargement was assessed in 19 adult patients who either had a nephrectomy (the removal of a nephron, 17 cases) or developed a functionless kidney following obstruction (two cases). Hypertrophy of the healthy kidney was quantified by comparing renal size on urography (X-ray after the injection of radiographic contrast material) before and after removal or destruction of the diseased kidney. 40% of the patients within the study showed compensatory enlargement, including (most surprisingly) two patients in their sixties. The average increase in length was 3% and the maximum increase in length was 9%. The results of the study showed that compensatory enlargement occurs during both adulthood and childhood. This contrasts with the initial belief that compensatory enlargement occurred only during childhood. The increase in kidney size is, however, significantly larger if the destruction or removal occurred earlier in life. The study also showed that the presence of a hypertrophied adult kidney over 17 cm in length usually indicates that the contralateral renal disease was present in childhood (affecting both the destroyed kidney as well as the previously healthy one). In summary, the kidney has a mechanism (though it is limited) to be able to compensate for both loss of nephrons, as well as a reduction in nephron efficiency, regardless of the cause. Bringing this back around towards my focus in this project, it shows that even if the tubular atrophy and interstitial fibrosis caused by BK virus nephropathy (see post on BK Virus Nephropathy) can never be repaired, by stopping or slowing the progression of the disease, the kidney can take steps to bring itself closer to its original functionality. The irreversibility of the damage still highlights the need for close monitoring of transplant patients’ grafts as well as preventatively creating the most balanced immunosuppressive regimen for the patient.
In a 2009 study, compensatory renal enlargement was assessed in 19 adult patients who either had a nephrectomy (the removal of a nephron, 17 cases) or developed a functionless kidney following obstruction (two cases). Hypertrophy of the healthy kidney was quantified by comparing renal size on urography (X-ray after the injection of radiographic contrast material) before and after removal or destruction of the diseased kidney. 40% of the patients within the study showed compensatory enlargement, including (most surprisingly) two patients in their sixties. The average increase in length was 3% and the maximum increase in length was 9%. The results of the study showed that compensatory enlargement occurs during both adulthood and childhood. This contrasts with the initial belief that compensatory enlargement occurred only during childhood. The increase in kidney size is, however, significantly larger if the destruction or removal occurred earlier in life. The study also showed that the presence of a hypertrophied adult kidney over 17 cm in length usually indicates that the contralateral renal disease was present in childhood (affecting both the destroyed kidney as well as the previously healthy one). In summary, the kidney has a mechanism (though it is limited) to be able to compensate for both loss of nephrons, as well as a reduction in nephron efficiency, regardless of the cause. Bringing this back around towards my focus in this project, it shows that even if the tubular atrophy and interstitial fibrosis caused by BK virus nephropathy (see post on BK Virus Nephropathy) can never be repaired, by stopping or slowing the progression of the disease, the kidney can take steps to bring itself closer to its original functionality. The irreversibility of the damage still highlights the need for close monitoring of transplant patients’ grafts as well as preventatively creating the most balanced immunosuppressive regimen for the patient.
I see that my question in the last post is answered here! Thanks, Alex.
ReplyDelete